O' 


\ 


0 


THE  LIBRARY 

OF 

THE  UNIVERSITY 

OF  CALIFORNIA 

LOS  ANGELES 

Gift  of 
Dr.  L.   C.  McLain 


AN   ATLAS 


OF  THE 


DIFFERENTIAL  DIAGNOSIS 


OF  THE 


DISEASES  OF  THE  NERVOUS  SYSTEM 

(WITH  A  PHYSIOLOGICAL  INTRODUCTION) 


ANALYIICAL  AND  SEMEIOLOGICAL 
NEUROLOGICAL  CHARTS 


BY 

HENKY  HUN,  M.  D. 

F  ORMERLY  PROFESSOR  OF  THE  DISEASES  OF  THE  NERVOUS  SYSTEM  IN  THE  ALBANY  MEDICAL  COLLEGE; 
MEMBER  OF  THE  AMERICAN  MIDICAL  ASSOCIATION, 

THE  ASSOCIATION  OF  AMERICAN  PHYSICIANS, 

THE  AMERICAN  NEL'ROLOGICAL  ASSOCIATION.  ETC.; 

AUTHOR  OF  "A  GUIDE  FOR  AMERICAN  MEDICAL  STUDENTS  IN  EUROPE." 

-SYLLABUS  OF  A  COURSE  OF  LECTURES  ON  THE  DISEASES  OF  THE  NERVOUS  SYSTEM,"  ETC. 


THIRD 
REVISED  AND  ENLARGED 

EDITION 


¥' 


THE  SOUTHWORTH  COMPANY,  PUBLISHERS 
TROY,  NEW  YORK 

1922 


v;:      ■' :„/ 


Copyrighted  1912,  1914  and  1922  by 
HENRY  HUN,  M.  D. 


Momedical 
library 


17 

1  ^_-, 


141 


To 

Thomas    Hun 

a  loving  father 

a  learned  physician 

a  man  of  wisdom  and  wit 

this  book  is  dedicated 

in  most  grateful  remembrance. 


»;^(wo35 


TABLE  OF  CONTENTS 


Preface,  Page  i 

PART  ONE 

SEM  BIOLOGY 

S. — Introduction  to  the  Semeiological  Charts. 

Methods  of  examination  of  patients  suffering  from  ner\'ous  diseases 
and  a  discussion  of  the  significance  of  symptoms. 


CHART 

I. 

II. 

III. 

IV. 

V. 
VI. 

VII. 
VIII. 


PAGE 

39. — Case  taking- 

57- 
61 
71 


85 

95 

105 

115 

IX.     119. 


examination  of  patients ;  comprising  numbers  i  to  80. 


. — Analysis  of  etiological  factors;  comprising  numbers  81  to  194. 

— Semeid<ogy  of  disordered  mental  activity ;  comprising  numbers  200  to  237. 

Senieiology  of  disordered  voluntary  motor  activity;  comprising  numbers  240  to 
294. 
, — Semeiology  of  disordered  reflex  activity ;  comprismg  numbers  296  to  341. 
. — Semeiology  of  disordered  sensory  activity ;  comprising  numbers  344  to  392. 
, — Electrical  examination;  comprising  numbers  393  to  403. 
, — Examination  of  cerebro-spinal  fluid ;  comprising  numbers  405  to  414. 

(  Special  syndromes;  comprising  numbers  415  to  456. 

>  .'\natomical  terms ;  comprising  numbers  460  to  465. 


127. 


X. 

XI. 

XII. 

133- 
141.- 
149.- 

XIII. 
XIV. 

165.- 

XV. 

185.- 

XVI. 
XVII. 

■95. 

205. 

CVIII. 

-2I5- 

XIX. 

217. 

XX. 

221  — 

XXI. 

229.- 

XXII. 

239-- 

FIGURE 

PAGE 

I  to  5. 

no. 

6. 

11.^- 

7  to  13. 

168. 

14. 

179. 

15  to  17. 

250-1 

18. 

252- 

19- 

253- 

20. 

254- 

21  to  23. 

255- 

24  and  26. 

256-7 

25- 

256. 

27. 

258. 

28  to  31. 

259. 

32. 

260. 

33- 

261. 

34- 

262. 

35- 

263. 

36. 

264. 

37- 

264. 

38. 

265. 

PART  TWO 

Diagnosis 

-Introduction  to  the  Diagnostic  Charts.    Clinical  classification  of  nervous 
symptoms  as  a  basis  for  diagnosis. 

-Diseases  causing  motor  paralysis  (vifeakness)  ;  comprising  numbers  469  to  557. 

-Diseases  causing  convulsion  or  spasm ;   comprising  numbers   570  to  632. 

-Diseases  causing  perversion  of  motion  (ataxia,  tremor,  nystagmus,  fibrillation, 
also  local  palsies  and  spasms)  ;  comprising  numbers  635  to  733. 

-Diseases  causing  disorders  of  speech  and  gait ;  comprising  numbers  735  to  804, 

-Diseases  causing  diminution  or  exaggeration  of  sensation  (anesthesia,  hy- 
peresthesia, etc.)  and  disorders  of  special  senses;  comprising  numbers  805 
to  928. 

-Diseases  causing  perversion  of  sensation  (pain  and  vertigo) ;  comprising  num- 
bers 930  to  1034. 

-Diseases  causing  mental  disorders;  comprising  numbers  1036  to  1120. 

-Diseases  causing  trophic  (change  of  size)  and  sympathetic  (ganglionic  and 
vaso-motor)    disorders;   comprising  numbers   1121   to   1203. 

-Diseases  caused  by  syphilis  of  the  nervous  system;  comprising  numbers  1205 
to  1217. 

-Diseases  associated  with  abnormal  cerebrospinal  fluid;  comprising  numbers 
1220  to   1244. 

PART  THREE 

LOCAUZATION 

■Localization  in  spinal  cord ;  comprising  numbers  1250  to  1279. 
•Localization  in  brain  ;  comprising  numbers  1290  to  1309. 

General  localization  from  symptoms  of  paralysis  or  spasm;  comprising  num- 
bers 1310  to  1415. 

PLATES 

Erb's  motor  points  for  electrical  examination. 

Erb's  diagram  showing  the  effects  of  injury  of  a  nerve. 

Diagrams  illustrating  the  various  laryngeal  paralyses. 

Diagram  illustrating  the  various  forms  of  ocular  paralyses. 

Diagrams  of  the  cerebral  hemispheres. 

Diagram  of  oculo-motor  nucleus. 

Diagram  of  nuclei  in  brain  stem. 

Diagram  of  section  through  pons  Varolii. 

Diagrams  of  sections  through  the  medulla  oblongata. 

Diagrams  of  transverse  sections  of  the  spinal  cord. 

Diagram  of  nuclei  in  anterior  horns  of  cord. 

Schematic  representation  of  the  more  important  diseases  of  the  spinal  cord. 

Schematic  representation  of  some  points  in  the  physiology  and  pathology  of 

the  spinal  cord  and  of  the  peripheral  nerves. 
Diagram  showing  the  motor  and  reflex  functions  of  the  spinal  cord  segments. 
Diagram  showing    the   cutaneous   distribution    of   the   sensory  nerves  and 

nerve  roots. 
Diagram  of  long  motor  projection  tracts. 
Diagram  of  long  sensory  projection  tracts. 
Diagram  showing  course  of  gustatory  fibers. 
Diagram  illustrating  hemianopia. 
Diagram  showing  the  nuclei  of  origin  and  the  distribution  of  all  motor  and 

sensory  nerves. 

INDEX,  Page  267 


PREFACE 


The  diagnosis  of  diseases  of  the  nervous  system  is  generally  r^arded  by 
medical  students  as  one  of  the  most  difficult  subjects  in  their  course  of  study. 
It  is  so  difficult  that  many  students  become  discouraged  and  after  a  few  attempts 
make  no  strong,  continued  effort  to  master  it  and,  perhaps  in  consequence,  physi- 
cians generally  are  weaker  in  this  than  in  other  phases  of  their  work.  In  the 
hope  of  making  this  task  less  difficult  for  both  physicians  and  students  this 
book  has  been  written.  If  the  student  can  be  taught  to  make  the  diagnosis  of 
these  diseases  with  comparative  ease,  it  may  happen  tliat  he  will  be  led  to  under- 
take those  further  studies  in  the  finer  anatomy  and  physiology  of  the  nervous 
system,  which  are  essential  for  a  full  understanding  of  this  difficult  but  fascinat- 
ing department  of  medicine. 

A  careful  physical  examination  and  history  of  the  case,  as  complete  as  can 
be  obtained,  are,  of  course,  the  essential  basis  of  every  diagnosis;  but  the  com- 
monly employed  method  of  comparing  the  combination  of  symptoms  thus 
obtained  in  any  case  with  the  various  syndromes  characteristic  of  the  different 
diseases  until  a  similar  combination  can  be  found,  is  not  altogether  satisfactory. 
More  scientific  and  instructive  are  the  analysis  of  each  important  symptom,  its  ex- 
planation in  the  normal  or  abnormal  activity  of  the  nervous  system  and  the  con- 
sequent ascertaining  of  the  disease  which  must  cause  it  under  the  circumstances 
(the  other  symptoms)  existing  in  any  individual  case  which  may  present  itself. 

In  spite  of  its  apparent  complexity,  the  diagnosis  of  nervous  diseases  lends 
itself  better  than  that  of  the  diseases  of  most  of  the  other  organs  to  exact  path- 
ological analysis.  Just  as  a  chemist  in  analyzing  a  substance  of  unknown  com- 
position by  a  series  of  appropriate  tests  eliminates  from  consideration  one  group 
of  chemical  bodies  after  another  until  he  finally  discovers  its  class  and  name,  so 
the  neurologist  subjects  a  patient  to  one  test  after  another  in  definite  sequence. 
As  the  result  of  each  test  he  throws  out  of  consideration  one  or  more  groups  of 
diseases  and  assures  himself  that  he  has  to  do  with  a  disease  belonging  to  another 
definite  group.  With  each  successive  test  the  number  of  diseases  constituting 
a  group  becomes  less,  until  finally  one  definite  individual  disease  stands  revealed 
among  the  few  most  closely  related  to  it  and  can  be  absolutely  identified  by  a  com- 
parison of  the  remaining  symptoms  characteristic  of  each,  which  are  given  in  the 
final  abstracts.  This  analytical  method  is  used,  I  think,  by  most  teachers  of  neu- 
rology in  demonstrating  cases  of  diseases  before  their  classes  of  students.  It  is  the 
crystallization  of  this  teaching  into  the  tabular  form  which  this  book  attempts  to 
present. 

In  using  this  book  for  diagnostic  purposes  it  is  important  that  the  "Intro- 
duction to  the  Diagnostic  Charts"  on  page  119  should  be  carefully  studied.  By 
means  of  these  charts  it  is  possible  to  diagnosticate  easily  and  rapidly  almost  any 


disease  of  the  nervous  system  and  to  localize  the  lesion,  when  any  lesion  exists.  If 
the  examiner  makes  a  mistake  at  any  point,  the  next  step  in  thei  process  or  the 
abstract  of  the  other  symptoms  of  disease  will  probably  show  him  that  he  is  in 
error  and  that  it  is  necessary  for  him  to  retrace  his  steps. 

For  the  sake  of  completeness  certain  trophic  diseases  are  included,  which, 
although  causing  a  number  of  functional  disturbances  in  the  nervous  system,  are 
not  really  nervous  diseases. 

As  might  naturally  be  expected,  the  same  disease,  in  so  far  as  it  presents 
many  symptoms,  appears  a  number  of  times  in  the  different  charts  and  even  in  the 
same  chart;  so  that,  in  order  to  get  a  more  complete  idea  of  its  symptomatology,  it 
is  essential  that  the  different  abstracts  of  it  should  all  be  read.  To  facilitate  this, 
cross  references  by  numbers  within  brackets  are  placed  in  the  text. 

Many  diagnostic  and  technical  terms  are  used  which  may  not  be  familiar  to 
the  student;  therefore  these  terms  are  classified,  defined  and  their  significance 
stated,  as  far  as  it  is  known  to  the  author,  in  a  series  of  semeiological  charts  pre- 
ceding the  diagnostic  ones.  Cross  reference  to  these  terms  also  is  facilitated  by  the 
numbers  within  the  brackets.     A  very  complete  index  serves  this  same  purpose. 

The  peculiar  characteristic  of  this  book  on  diagnosis  is  that  it  gives  to  the 
student  or  physician  a  key  by  which,  in  a  comparatively  easy  manner  from  one  or 
more  important  symptoms,  he  can  arrive  at  a  diagnosis.  It  also  has  the  advantage 
that  it  divides  the  diseases  into  groups,  the  members  of  which  have  a  definite 
relationship  with  each  other;  so  that  in  the  process  of  using  the  charts  the  student 
is  constantly  catching  glimpses  of  the  natural  relationships  between  the  different 
diseases  of  the  nervous  system.  Although  the  symptoms  of  different  diseases  have 
often  been  contrasted  in  tables  of  parallel  columns,  in  no  other  book,  known  to  the 
author,  has  the  subject  been  presented  as  it  is  here,  and  this  must  be  his  excuse 
for  publishing  it  and  for  any  defects  which  it  may  show,  as  there  was  no  model 
which  could  be  followed  in  preparing  it. 

In  the  preparation  of  this  book  the  author  ha?  received  valuable  suggestions 
and  aid  from  several  friends  and  especially  from  Drs.  Archambault,  Dawes, 
Hawn,  Mosher,  Streeter  and  Viets.  To  these,  his  present  friends  and  former 
students  and  assistants,  he  gratefully  acknowledges  his  indebtedness  and 
returns  his  thanks. 

It  is  very  gratifying  to  the  author  that  the  first  two  editions  of  five  thousand 
copies  have  been  exhausted,  giving  him  an  opportunity  of  making  a  complete  re- 
vision of  the  text,  and  of  making  a  few  additions  both  to  the  semeiological  and  to 
the  diagnostic  charts,  which  seem  to  him  to  add  much  to  the  value  of  the  work. 

The  criticisms  of  Dr.  Mosher  and  his  untiring  aid  in  putting  the  three  editions 
through  the  press  are  large  factors  in  whatsoever  success  the  book  may  have. 


Henry  Hun. 


Albany,  N.  Y., 

March  1,  1922. 


PART  I 

SEMEIOLOGY 
THE  EXAMINATION  OF  PATIENTS 

AND  A 

PHYSIOLOGICAL  AND  PATHOLOGICAL  ANALYSIS 

OF  THE 

RESULTS  OBTAINED  FROM  SUCH  EXAMINATION 


AN  ANALYSIS  OF  THE 
SUBJECTIVE  AND  OBJECTIVE  SYMPTOMS  OF  DISEASE 


Introduction  to  the  Semeiological  Charts 

A   Review  of  the   Physiology  of  the  Nervous  System 
(The  bracketed  numbers  refer  to  the  numbers  in  the  body  of  the  book) 


The  diagnosis  of  nervous  diseases,  if  it  is  to  be  at  all  satisfactory  and  accurate,  must  be  based 
on  anatomy  and  physiology.  It  might  seem  strange  to  mention  physiology  in  connection  with  such  a 
schematic  tabulation  of  diagnosis  as  this  book  presents.  All  of  these  charts,  however,  are  con- 
structed strictly  on  a  physiological  basis  and  without  such  basis  they  could  not  have  been  made  or 
could  not  be  successfully  used.  The  diminution,  exaggeration,  or  perversion  of  the  different  phy- 
siological functions  of  the  nervous  system  constitutes  the  scheme  of  each  chart  and  is  the  key  for 
the  diagnosis  of  the  separate  diseases  which  are  their  clinical  expression.  The  practitioner  is  sup- 
posed to  have  some  acquaintance  with  these  subjects,  and  the  curriculum  of  the  medical  college  is 
so  arranged  that  the  student  is  taught  them  before  he  commences  clinical  work.  It  seems,  however, 
desirable  to  make  here  an  attempt  to  present  a  very  brief,  but  comprehensive,  outline  of  the 
physiology  of  the  nervous  system,  including  some  statements  as  to  its  anatomy,  which  latter  can 
be  supplemented  by  an  inspection  of  the  plates  at  the  end  of  the  book. 

The  human  being  is  a  unit  in  the  universe  which  contains  him,  of  which  he  is  a  part  and  with 
which  he  is  in  constant  relationship.  Life  consists  in  a  constant  reaction  of  the  organism  to  the 
forces  of  nature  which  act  upon  it  from  all  sides.  These  reactions  are  called  "physiological  ac- 
tivities," and  when  they  become  disordered  from  any  cause  they  are  called  "pathological  activities," 
or  symptoms  of  disease;  when  they  are  altogether  absent  the  organism  is  dead.  The  nervous  sys- 
tem is  the  most  important  seat  of  these  reactions.  Of  the  numerous  forces  and  forms  of  energy 
in  the  world  only  a  portion  can  be  perceived  by  man.  It  is  certain  that  some  animals  perceive 
things  imperceptible  to  him. 

The  various  forms  of  energy  in  nature  cannot  act  directly  upon  the  nervous  system  to  produce 
sensory  impulses;  but  intermediate  organs,  "end-organs,"  or  "receptors,"  are  necessary  to  trans- 
mute into  nervous  energy,  the  external  energy  (sun's  rays,  etc.)  which  comes  from  the  external 
world.  There  may  be  some  question  whether  the  external  energy  passes  through  the  nervous  sys- 
tem to  the  muscles  and  from  them  passes  out  again  to  the  external  world;  or  whether  the  external 
energy  (light,  etc.),  in  its  action  upon  the  end-organ,  liberates  the  potential  energy  stored  in  the 
end-organ,  just  as  a  spark  liberates  the  potential  energy  stored  in  gunpowder.  The  latter  assump- 
tion seems  to  be  the  triie  one,  because  the  energy  imparted  to  the  animal  by  the  stimulus  is 
much  less  than  the  consequent  energy  manifested  by  the  animal.  Hence  the  conclusion,  that  in 
virtue  of  chemical  changes  the  potential  energy  stored  in  the  end-organ  becomes  active;  the  ex- 
citing cause  of  this  being  the  external  force  or   foreign  irritation. 

There  are  doubtless  many  forms  of  energy  in  the  world  which  cannot  be  perceived  by  man 
because  he  possesses  no  suitable  end-organs  to  bring  about  this  transmutation.  Sometimes 
this  can  be  accomplished  by  adding  to  the  end-organs  some  mechanical  contrivance  suitable  to 
bring  about  this  transmutation ;  as,  for  instance,  the  fluoroscopic  screen  for  X-rays.  The  universal 
ether  is  doubtless  in  vibration  far  beyond  the  limits  of  about  four  hundred  million  million  per 
second,  which  constitute  the  color  red  and  about  seven  hundred  and  sixty  million  million,  which 
constitute  violet;  and,  indeed,  we  have  reason  to  believe  that  the  ultra-violet  rays  have  some  eflfect 
upon  the  human  body,  but  beyond  the  above  limits  the  vibration  of  the  ether  is  neither  reacted  to  by 
our  eye  nor  recognizable  by  our  brain.  The  sensory  apparatus  is  not  perfect.  Some  time  is  required 
for  the  excitation  caused  by  the  external  stimulus  to  pass  through  the  end-organ  and  the  nerve 
fibers  to  the  cerebral  cortex  and  to  excite  the  latter  to  action  (the  initial  lag)  and  the  resulting  sen- 
sation persists  an  even  longer  time  after  the  external  stimulus  has  ceased  (the  terminal  lag). 
Things  moving  very  rapidly,  as  for  instance  the  spokes  of  a  rapidly  moving  wheel,  cannot  be 


seen  individually,  and  a  rapidly  recurring  series  of  the  same  sound  blends  into  a  musical  tone. 
But,  however  limited  and  imperfect  the  sensory  apparatus  may  be,  the  end-organs,  each  of  which  is 
specific  and  can  respond  to  one  definite  form  of  energy  and  to  that  one  only,  whether  on  the  sur- 
face or  in  the  interior  of  the  body,  are  starting  points  from  which  all  nervous  and  mental  activity, 
even  the  highest,  springs.  The  fundamental  function  of  the  end-organ  and  hence  the  primary 
activity  of   the  nervous  system  is,   thus,   "receptivity." 

The  fundamental,  anatomical  element,  or  unit,  of  the  nervous  tissue  is  the  "neuron" (461-4)  : 
&  nucleated  cell  with  many  processes  projecting  from  it,  some  short  and  branching  (dendrons)  ; 
one  (rarely  two  or  more),  often  extending  a  long  distance,  usually  becomes  the  axon  of  a 
medullated  nerve  fiber,  and  frequently  gives  ofif  a   few  collateral  branches. 

Both  axons  and  dendrons  are  composed  of  delicate  fibrillae  which  pass  directly,  without  inter- 
ruption, through  the  cell  body  from  the  tip  of  a  dendron  to  the  tip  of  the  axon.  Of  these  neurons, 
varying  in  form  and  size  and  supported  by  the  delicate  framework  of  the  neuroglia,  the  entire 
nervous  system  is  composed. 

The  fundamental  physiological  characteristics  of  the  nervous  tissue  are  excitability  and  trans- 
mission :  the  power  of  receiving  an  excitation  and  transmitting  it  from  one  end  of  the  neuron  to  the 
other,  and  even  to  other  neurons  with  which  the  first  has  anatomical  and  physiological  relation- 
ship, or  contact.  By  its  dendrons  the  nerve  cell  receives  nervous  impulses  and  by  its  axon  trans- 
mits these  impulses.  The  transmission  of  energy  from  one  neuron  to  another  at  their  synapse,  or 
point  of  contact,  depends,  probably,  upon  differences  in  the  tension  of  this  energy  in  the  two  neu- 
rons. Later  observations,  however,  seem  to  prove  that,  at  the  termination  of  the  axon,  its  fibrillae 
jjass  directly  into  the  dendron  of  another  neuron,  at  least  in  some  cases.  A  neuron  is  merely  a 
conducting  channel.     It  originates  nothing.     It  merely  transmits. 

The  rapidity  of  conduction  of  the  nervous  impulse  along  a  nerve  fiber  is  approximately  foui 
hundred  feet  per  second  normally,  but  varies  with  the  temperature  and  other  artificial  conditions. 
The  nervous  conduction  seems  to  be  a  wave  of  chemical  decomposition  associated  with  a  local  elec- 
trical current.     The  transmission  of  an  impulse   from  one  neuron  to  another  is  relatively  slow. 

The  Centripetal  Neurons 

Cutaneous  Sensibility.  The  surface  of  the  body  and  the  cavities  connected  with  it  contain  organs:  the 
terminal  organs  of  sense  (the  sensory  "end-organs"),  which  bring  the  body  into  connection  with  some,  but 
probably  far  from  all,  of  the  forces  of  nature  and  these  end-organs  are  so  constructed  as  to  transmute  physi- 
cal forces  (light  in  the  eye,  sound  in  the  ear,  heat,  cold,  touch,  pressure  and  pain  in  the  skin,  etc.,)  into  nervous 
excitations  in  the  terminal  filaments  of  the  peripheral  nerves.  The  skin  contains  many  of  these  isolated 
terminal  sense  organs  and,  therefore,  sensibility  is  not  spread  uniformly  over  the  skin,  as  it  appears  to  be,  but 
is  really  located  in  individual  points  lying  close  together,  but  each  distinct.  From  these  points  of  greatest  sen- 
sibility its  acuteness  diminishes  concentrically.  In  every  square  centimeter  of  skin  there  are,  on  the  average, 
12  to  13  points  for  cold,  o  to  3  for  heat,  and  24  for  tactile  impressions;  although  these  figures  vary  very  greatly 
for  different  parts  of  the  skin,  the  points  being  most  numerous  on  the  finger  tips  and  fewest  on  the  back. 
Points  for  tactile  impressions  vary  from  7  to  300  per  square  centimeter.  There  are  also  distinct  points  for 
painful  sensibility.  These  points  for  painful  sensibility  are  much  more  numerous,  but  far  less  sensitive  and 
delicate,  than  are  those  for  tactile  sensibility.  The  nerve  fibers  supplying  these  points  of  painful  sensibility 
have  no  end-organs, but  end  as  fine  free  filaments.  Where  the  skin  is  stretched  over  bone  ((T.g.,  the  malleoli)  tactile 
sensibility  is  less  distinct,  and  it  is  more  distinct  where  the  skin  is  hairy ;  a  point  for  tactile  sensibility  being 
situated  at  the  base  of  most,  if  not  of  all,  hairs.  There  may  be  a  delay  in  the  conduction  of  painful  impressions 
through  either  the  neuron  or  the  synapse;  so  that  with  repeated  pin-pricks  the  pain  becomes  more  acute  (sum- 
mation of  impulses).  After  section,  or  injury,  of  a  nerve,  the  anesthesia  and  analgesia  are  never  so  extensive 
as  is  the  area  of  distribution  of  the  nerve,  and  sensibility  often  returns  before  the  regeneration  of  the  nerve 
has  completely  taken  place.  This  is  partly  due  to  peripheral  anastomoses  with  terminal  filaments  of  adjacent 
nerves  and  partly,  perhaps,  to  sensory  fibers  in  the  motor  nerves   (recurrent  sensibility.) 

Head  and  his  colleagues,  after  much  experimental  work  on  the  subject,  arrived  at  the  following  con- 
clusions : 

There  are  in  the  peripheral  areas  three  kinds  of  sersibility,  due  to  there  being  three  different  kinds  of  nerve 
fibers  supplied  to  each  area : 

1st.  Deep  Sensibility:  Muscle  sen.se,  joint  sense,  pressure,  pain,  and  vibration  sense.  This  sensibility  is 
conveyed  by  sensory  nerve  fibers,  more  or  less  deeply  situated  beneath  the  .skin,  and  usually  running  with  the 
motor  nerves.  When  the  nerves  of  the  tendons  are  cut.  these  forms  of  sensibility  are  lost,  but  not  on  section 
of  the  sensory  nerves  of  the  skin. 


2nd.  Eficritic  Sensibility:  Tactile  sensibility  for  slight  impressions,  form  and  space  sense,  sense  ot 
moderate,  not  extreme,  temperatures,  (22°  to  40°  C.)  and  the  precise  localization  of  pain  and  temperature 
sense.  This  area  of  sensibility  is  very  constant  for  each  individual  nerve.  The  restitution  of  this  form  of  sen- 
sibility is  very  slow  and  is  not  complete  until  several  years  after  the  injury  to  the  nerve. 

3d.  Protopathic  Sensibility:  Pain  and  sense  of  extremes  of  temperature  (below  22°  or  above  40°  C). 
Disturbances  of  this  form  of  sensibility  are  accompanied  by  paresthesiae  and  a  false  localization.  This  form 
of  sensiblity  is  best  tested  on  the  periphery  of  the  affected  area,  where  the  anesthesia  is  not  complete,  or  over 
the  whole  area  while  the  regeneration  is  taking  place.  The  restitution  of  this  form  of  sensibility  is  relatively 
rapid    (7   to    10  weeks). 

These  researches  of  Head  are  of  great  interest  and  value  and  have  attracted  much  attention  and  discussion: 
but  they  are  not,  in  their  entirety,  accepted  by  all  neurologists  and  more  recent  investigations  seem  to  show  thit 
after  section  or  injury  of  a  nerve  all  forms  of  sensation  are  practically  equally  impaired  and  in  cases  of  re- 
covery all  return  with  equal  rapidity ;  so  that  testing  for  one  form  usually  suffices  for  all.  The  testing  of  sensi- 
bility is  very  difficult,  so  much  depends  upon  the  patient's  intelligence,  power  and  quickness  of  perception  and 
freedom  from  suggestion. 

Sensory  impulses  of  all  kinds  are  carried  to  the  central  nervous  organs  by  the  sensory  nerves.  Of  these, 
the  spinal  nerves  enter  the  cord  (mainly)  through  their  cell  bodies  in  the  spinal  ganglia  and 
through  the  posterior  nerve  roots  (Fig.  26)  ;  while  the  fibers  of  the  trigeminal,  the  great  cranial 
nerve  supplying  sensation  to  the  face,  after  passing  through  their  cell  bodies  in  the  Gasserian  ganglion, 
enter  the  pons  (Fig.  ig).  The  fibers  from  the  posterior  nerve  roots,  on  entering  the  spinal  cord,  are  sorted  ac- 
cording to  their  physiological  function  into  three  great  groups  (Fig.  26).  One  group  which  conveys  most  of 
the  tactile,  and  a  part  of  the  pressure  and  muscle-joint  sense  impressions,  ascends  mainly,  without  decussating, 
in  the  posterior  columns  to  the  nuclei  of  the  columns  of  Goll  and  Burdach,  and  thence  is  continued  by  a  new  set 
of  neurons  (the  internal  arcuate  fibers),  which  decussate  and  pass  through  the  median  lemniscus  (fillet)  (Figs. 
20-3)  to  the  optic  thalamus;  whence  it  is  continued,  also  by  another  set  of  neurons  (relays),  to  the  parietal 
cortex.  These  fibers  convey  impulses  essential  to  the  production  of  association  reflexes.  The  second  group, 
which  conveys  impulses  essentia!  to  the  maintenance  of  equilibrium,  passes  to  the  cells  of  the  columns  of 
Clarke  and  thence,  mainly  without  decussating,  through  the  direct  cerebellar  (posterior,  spino-cerebellar  or 
Flechsig's")  tract  in  the  outer  part  of  the  lateral  column  and  through  the  restiform  body  to  the  vermis  or  middle 
lobe  of  the  cerebellum.  The  third  group,  which  conveys  all  the  temperature  and  painful  impressions,  passes 
through  cells  in  the  posterior  horn,  decussates  in  the  central  gray  matter  of  the  cord  and  passes  upward 
through  the  spino-thalamic  tracts  and  lateral  portion  of  the  formatio  recticularis,  joining  in  part  the  median 
lemniscus,  to  the  optic  thalamus  and  thence  to  the  parietal  cortex,  and  in  part  coursing  backwards  to  the  cere- 
bellum. The  fibers  of  the  first  and  third  group  have  thus  a  double  ending,  one  in  the  optic  thalamus  and  cue 
in  the  cortex. 

A  destructive  lesion,  either  in  the  terminal  end-organ  or  at  any  point  of  these  sensory  tracts  or  neurons, 
causes  a  corresponding  paralysis  of  sensation  (anesthesia)  :  while  a  slight,  irritative  lesion  may  cause  hyperes- 
thesia, paresthesiae  or  pain  in  the  distribution  of  the  nerve. 

In  addition  to  the  anesthesia,  which  occurs  in  organic  disease  of  the  nervous  system,  there  is  an  anesthesia 
which  occurs  in  hysteria;  hysterical  anesthesia  (415).  This  hysterica!  anesthesia  occasionally,  but  rarely,  in- 
volves the  organs  of  special  sense.  It  more  commonly  involves  cutaneous  sensibility  and  then  the  anesthesia 
is  not  limited  to  the  distribution  either  of  a  peripheral  nerve  or  of  a  nerve  root.  It  may  instantaneously  disap- 
pear. It  may  recur  in  the  same  place,  or  in  some  other  locality.  It  does  not  prevent  the  use  of  the  part  in  per- 
forming acts  in  which  sensibility  is  essential.  Upon  excitation  of  the  hysterical  anesthetic  parts  vascular  re- 
flexes occur,  which  is  never  the  case  in  anesthesia  due  to  organic  disease,  peripheral  or  spinal.  It  is  evident 
that  this  hysterical  anesthesia  is  a  purely  mental  phenomenon :  an  imagined  idea  or  delusion.  It  is  due  to  sug- 
gestion ;  a  "fixed  idea"  is  so  dominant  that  the  sensation  of  pain  or  touch,  which  should  normally  result,  dots 
not  enter  consciousness  (see  later).  The  excitation  causing  the  dominant  fixed  idea  inhibits  other  cortical 
activity. 

Pain  (374)  is  an  unpleasant  sensation  which  never  occurs  in  health,  but  only  when  the  body  is  injured, 
either  mechanically  or  chemically.  It  is  a  signal  or  warning  that  the  body  needs  protection.  Its  intensity  de- 
pends not  only  upon  the  intensity  of  the  mechanical  or  chemical  irritation,  but  also  upon  the  condition  (inflam- 
matory, etc.)  of  the  peripheral  nerves  or  of  the  cerebral  cortex.  It  is  more  intense  when  cerebral  cellular 
activities  produce  the  concepts  of  fear  and  apprehension  and  the  condition  of  "active  attention"  (see  later), 
which  makes  the  painful  sensation  more  acute.  An  unexpected  wound  is  less  painful  than  an  anticipated  one. 
and  a  wound  is  often  not  at  all  painful  when  the  cortical  activity  is  greatly  excited  by  some  other  cause  (a 
battle  for  instance.)  Pain  is  often  associated  with  the  allied  perceptions  called  "paresthesiae"  (375), 
which  at  times  accompany,  and  at  times  follow,  the  pain  and  which  are  usually  of  central  origin  and  are  due  to 
irritation  of  the  sensory  fibers  at  some  part  of  their  course  through   the  central   nervous   organs. 

The  Kinesthetic  Sense  (43).  The  muscles,  tendons  and  articular  surfaces  all  contain  end-organs  which 
send  impulses  to  the  central  nervous  organs  whenever  the  muscles  contract  or  the  joints  move  and  cause  sen- 
sations from  which  the  position  of  the  limb  in  space  can  be  accurately  located,  even  when  the  eyes  are  closed 
or  the  patient  is  blind.  These  sensations  are  caused  by  the  movement  of  the  part  and  have  much  to  do  with 
regulating  and  inciting  its  further  movements.     The  kinesthetic  sense  is  of  the  greatest  importance  in  all  act- 

7 


ions  and  more  especially  in  the  automatic  and  habitual  acts,  (walking,  swimming,  talking,  singing,  etc).  The 
pathways  for  the  nerve  fibers  conducting  "muscle-sense,"  as  it  is  often  called,  and  which  have  their  origin  in  the 
muscle  spindles,  etc.,  enter  the  spinal  cord  through  the  posterior  nerve  roots,  mainly  pass  forwards  to  the  col- 
Bmns  of  Lockhart  Clarke  and  thence  directly  outwards  to  the  direct  cerebellar  tract  (posterior  spino-cerebellar 
tract)  and  through  it  to  the  cerebellum,  and  in  part  through  the  posterior  columns  to  the  cerebrum.  The 
corresponding  fibers  in  the  cranial  nerves  enter  the  pons  and  medulla. 

The  EquiUbrimn  Sense.  The  three  semi-circular  canals,  each  lying  in  a  plane  at  right  angles  to  the  other 
two,  constitute  the  most  important  organ  for  the  equilibration  of  the  body.  In  every  movement  of  the  head  the 
endolymph  in  the  canal  in  the  plane  in  which  the  head  is  moved  is  set  in  motion  and  moves  also  the  hair-cells 
in  the  canal.  The  stimulus  arising  from  these  irritated  hair-cells  passes  through  the  vestibular  branch  of  the 
acoustic  nerve  to  Deiter's  nucleus  and  its  neighborhood  and  thence  to  the  vermis  of  the  cerebellum.  The  vesti- 
bular nerve  has  no  direct  connection  with  the  cerebral  cortex  and  hence  its  activity  is  entirely  unconscious. 

Gustatory  Sensation.  (Charts  Via  and  XlVe).  The  mucous  membrane  of  the  mouth  (in  addition  to  the 
terminal  organs  for  tactile,  pressure,  thermic,  painful,  etc.,  impressions)  contains  also  the  terminal  organs  of 
the  nerves  of  taste:  the  taste-buds  or  bulbs,  so  called  from  their  form,  embedded  in  the  epithelium  of  the 
mucous  membrane  of  the  mouth,  especially  in  the  tip  and  edges  of  the  tongue.  Excitation  of  these  taste- 
bulbs  gives  rise  to  four  distinct  gustatory  sensations :  sweet,  acid,  salty  and  bitter,  to  which  may,  perhaps,  be 
added  alkaline  and  metallic.  Many  so-called  tastes  are  really  a  combination  of  gustatory  and 
olfactory  sensations.  The  nerve  fibers  arising  from  the  taste-bulbs  on  the  posterior  portion  of  the 
tongue  pass  by  the  glosso-pharyngeus  nerve  in  a  direct  manner  through  the  petrous  ganglion  to  their 
nucleus  in  the  medulla,  whence  they  ascend  with  the  other  sensory  fibers  of  the  lemniscus  to  the  optic  thal- 
amus, and  thence  to  the  cerebral  cortex,  posterior  to  the  olfactory  area,  in  the  gyrus  hippocampi,  (Fig.  i6) ; 
while  the  nerve  fibers  arising  from  the  taste  bulbs  on  the  anterior  portion  of  the  tongue  pass  at  first  in  the 
chorda  tympani  nerve  and  run  with  it  through  the  Fallopian  canal  to  the  geniculate  ganglion.  Here  the  fibers 
divide;  a  part  continuing  alongside  the  facial  nerve  and  forming  the  nervus  intermedius,  which  runs  to  a  nu- 
cleus in  the  medulla,  close  to  the  glosso-pharyngeal  nucleus ;  while  the  rest  of  the  fibers  run  through  the  petrosal 
nerve  and  join  the  fifth  nerve  and  pass  to  the  Gasserian  ganglion  (Fig.  36),  and  thence  to  the  cerebral  cortex 
(Fig.  16).  A  destructive  lesion  at  any  part  of  this  course  will  cause  unilateral  loss  of  taste  (ageusia). 
When  the  lesion  is  in  the  Fallopian  canal,  the  ageusia  may  be  associated  with  facial  paralysis  on  the  same 
side. 

Olfactory  Sensation.  (Charts  Via  and  XlVe).  The  mucous  membrane  of  the  nose,  analogous  to  that 
of  the  mouth,  in  addition  to  the  end-organs  for  tactile,  thermic,  pressure  and  painful  impressions,  contains  also 
the  end-organs  of  the  nerves  of  smell.  The  nerves  terminating  in  these  organs  pass  upward  through  the  crib- 
riform plate  to  the  olfactory  bulb,  and  thence  backward  through  the  olfactory  tract;  some  to  the  anterior  per- 
forated space  and  sub-thalamic  region  (for  the  olfactor>-  reflexes)  and  others  to  the  cortical  centers  for  smell 
in  the  coniu  Ammonis  (Fig.  16).  These  fibers  do  not  pass  through  the  internal  capsule  as  do  the  fibers  from 
all  the  other  organs  of  sense,  with  the  doubtful  exception  of  the  gustatory  fibers. 

Hearing.  (Charts  Via  and  XI Ve).  The  terminal  organ  for  hearing  is  the  organ  of  Corti  in  the  cochlea 
within  the  petrous  portion  of  the  temporal  bone.  In  this  organ  there  is  a  long  series  of  vibratory  structures  of 
unequal  length  supported  upon  the  basilar  membrane  (membrana  spiralis)  ;  so  that  among  them  can  be  found 
a  representative  for  every  possible  tone  (produced  by  single  vibrations  of  any  rapidity  between  40  and  40,000 
per  second)  with  its  overtones,  or  harmonics.  The  acoustic  nerve  (cochlear  nerve)  arising  in  this  organ 
passes  to  the  ventral  and  dorsal  acoustic  nucleus  in  the  pons  (Fig.  19).  From  this  nucleus 
fibers  pass  upward,  some  decussating  and  some  not,  through  the  lateral  fillet  (lemniscus  lateralis)  to  the  posterior 
corpora  quadrigemina  and  the  median  geniculate  body  ofthe  thalamus  and  thence  through  the  sublenticular 
region  of  the  internal  capsule,  posterior  to  the  fibers  for  cutaneous  sensibility,  and  reach  the  cortical  auditory 
area  in  the  anterior  transverse  temporal  convolution  immediately  below  and  forming  the  lower  margin  of  the 
Sylvian  fissure  in  each  hemisphere.  A  destructive  lesion  of  one  acoustic  nerve  will  cause  unilateral  deafness 
on  the  same  side,  but  a  lesion  of  the  tract  connecting  the  subcortical  with  the  cortical  centers,  since  this  tract 
contains  Ixjth  crossed  and  uncrossed  fibers,  will  not  cause  any  deafness  The  cortical  representation  of  the  au- 
ditory nerve  is  bilateral.  Deafness  results  only  from  ,1  bilateral  central  lesion  affecting  the  corpora  quadri- 
gemina or  the  subcortical  tracts  described  above.  Even  destruction  of  the  acoustic  cortical  center  in  both  hemi- 
spheres does  not  seem  always  to  cause  complete  deafness. 

Sight  (Charts  Via  and  XIV,  b,  c,  d).  The  terminal  end-organs  for  sight  consist  of  the  rods  and  cones 
in  the  retina.  The  rods  seem  to  be  concerned  with  seeing  in  dim,  the  cones  in  bright,  light.  They  vary  in 
relative  numbers  in  different  animals,  according  as  the  latter  roam  by  night  or  by  day.  They  also  vary  in  man 
according  to  their  situation.  Only  cones  are  found  in  the  fovea  centralis.  These  gradually  diminish  in  num- 
ber towards  the  periphery  of  the  retina,  where  only  rods  are  found.  From  these  structures  start  the  terminal 
filaments  of  the  optic  nerves,  which  run  backward  from  the  eyeballs  to  the  optic  chiasm.  In  the  optic  chiasm 
the  fibers  from  both  maculae  luteae  and  from  the  nasal  half  of  each  retina  decussate;  so  that  in  the  left  optic 
tract  are  collected  all  the  fibers  from  the  left  half  of  each  retina  (right  visual  field)  and  those  from 
both  maculae  luteae ;  while  in  the  right  optic  tract  are  collected  all  the  fibers  from  the  right  half  of  each  retina 
(left  visual  field)  and  those  from  both  maculae  luteae.     The  fibers  of  the  optic  tract  on  each  side  terminate  in 

8 


the  external  geniculate  body,  the  pulvinar  and  the  anterior  quadrigeminal  body  of  the  same 
side,  and  are  thence  continued  through  the  posterior  portion  of  the  internal  capsule  and  the  fasciculus  of  Gm- 
tiolet  to  the  lips  of  the  calcarine  fissure  on  the  median  surface  of  the  occipital  lobe  of  the  same  side  (Figs.  i6 
and  37). 

A  destructive  lesion  of  the  optic  nerve  causes  blindness  of  the  corresponding  eye,  but  a  lesion  of  any  por- 
tion of  the  optic  tract,  or  geniculate  body,  or  fasciculus  of  Gratiolet,  or  the  lips  of  the  calcarine  fissure,  will 
cause  homonymous  hemianopia  of  the  field  of  vision  of  the  opposite  side.  A  lesion  of  the  central  portion  of 
the  optic  chiasm  will  cause  bitemporal  hemianopia;  while  a  lesion  of  the  outer  edge  of  the  optic  chiasm  will 
cause  nasal  hemianopia  of  the  field  of  vision  of  the  opposite  side. 

Internal  or  General  Sensation.  In  addition  to  these  sensory  impulses,  which  convey  to  the  brain  excita- 
tions from  the  special  sensory  organs  and  hence  from  the  external  world,  there  are  others  which  come  from 
the  different  organs,  or  viscera,  of  the  body  and,  in  case  they  reach  the  cortex,  give  rise  to  what  are  called  in- 
ternal or  general  sensations.  Some  of  these  internal  excitations  remain  entirely  peripheral  and  affect  mainljr 
the  blood  vessels;  others  reach  no  further  than  the  spinal  cord  or  ganglia  at  the  base  of  the  brain  and  incite 
those  automatic  acts  which  preserve  the  nutrition  and  the  life  of  the  individual, and  still  others  reach  the  cere- 
bral cortex  and  at  times  affect  profoundly  the  processes  taking  place  in  it.  These  general  sensations  have 
much  influence  on  a  person's  moods,  thoughts  and  actions  and  especially  his  emotions.  Hunger  may  en- 
tirely alter  the  acts  of  a  man  or  beast. 

Such  internal  or  general  sensations  are  for  the  most  part  ill-defined  and  ill-localized.  They  seem  to  de- 
pend upon  the  blood  supply  and  the  activity  of  the  different  organs  and  upon  the  state  of  contraction  of  the 
hollow  organs;  and  they  appear  to  have  much  to  do  with  our  feeling  of  comfort  or  discomfort,  which  latter 
may  amount  to  great  pain.  The  sensation  of  hunger  seems  to  be  caused  by  contraction  of  the  empty  stom- 
ach, and  the  various  colics  by  contraction  of  the  circular  muscular  fibers  of  the  intestine,  the  ureter,  or  the 
bile  duct.  But  the  best  understood  of  all  these  internal  or  general  sensations  is  the  composite  one  called 
"muscle-joint  sense,"  which  is  mainly  made  up  of  impulses  from  the  muscle  and  its  tendon  and  the  articu- 
lating surfaces  and  also  from  impulses  from  the  skin  and  other  tissues  in  the  neighborhood,  as  these  are 
stretched  or  relaxed  in  motions  of  the  joint.  The  muscle-joint  sensory  conduction  we  have  already  considered 
under  the  term  of  the  kinesthetic  sense. 

The  centripetal  neurons  entering  the  spinal  cord  through  the  posterior  nerve  roots  are  very  numerous, 
being  about  one  and  a  third  million  in  man;  while  the  centrifugal  neurons  leaving  the  spinal  cord  through 
the  anterior  nerve   roots  number  less  than  one-half  a  million. 

The  Centwfugai,  Neurons 

Tlie  Louver  Motor  Neurons.  From  the  nerve  cells  in  the  anterior  horns  of  the  spinal  cord  axons  pass 
outwards  constituting  the  anterior  nerve  roots  and  run,  some  to  the  muscles  of  the  body,  others  to  the  ganglia 
of  the  sympathetic  system  and  others  to  the  glands. 

The  Upper  Motor  Neurons.  From  the  nerve  cells  in  the  anterior  central  convolution  (precentral  gyrus) 
axons  descend  through  the  corona  radiata  and  constitute  the  anterior  two-thirds  of  the  posterior  limb  of 
the  internal  capsule.  Thence  they  descend  through  the  crura  cerebn  and  the  pons  and  constitute  the  anterior 
pyramids  of  the  medulla  oblongata.  Hence  these  upper  motor  neurons  constitute  what  is  called  the  "pyram- 
idal tract,"  also  called  the  "fasciculus  cerebro-spinalis.  "  From  the  lower  part  of  the  medulla  a  small  part  of 
the  fibers  of  the  pyramidal  tract  pass  directly  downward  throughout  the  spinal  cord,  lying  on  the  median  sur- 
face of  the  anterior  colunm  (fasciculus  cerebro-spinalis  anterior  or  the  direct  pyramidal  tract)  ;  while  by  far 
the  larger  part  of  these  fibers  of  the  pyramidal  tract  decussate  and  pass  downward  throughout  the  spinal 
cord  in  the  lateral  column  of  the  opposite  side  (fasciculus  cerebro-spinalis  lateralis  or  the  crossed  pyramidal 
tract.  The  relative  size  of  the  direct  and  the  crossed  pyramidal  tract  varies  somewhat  and,  in  extremely 
rare  cases,  it  has  been  claimed,  no  decussation  of  the  pyramidal  tract  occurs.  On  the  other  hand  in  15% 
of  men  decussation  is  complete  and  there  is  no  direct  pyramidal  tract.  The  fibers  of  both  the  crossed 
and  the  direct  pyramidal  tracts  (the  fibers  of  the  direct  tract  decussating  in  the  anterior  white  commissure) 
finally  ramify  with  the  dendrons  of  the  nerve  cells  in  the  anterior  horn  on  the  opposite  side  of  the  body  from 
the  cerebral  hemisphere  in  which  these  fibers  originate. 

The  cortico-rubral  tract  consists  of  fibers  from  the  cortex  of  the  frontal  lobes  to  the  red  nucleus. 

The  cortico-pontile  tract  consists  of  fibers  from  the  cerebral   cortex  to  the  pons. 

The  thalamo-spinal  tract  consists  of  fibers  from  the  nerve  cells  in  the  optic  thalamus,  their  axons  passing 
downwards  and  terminating  near  the  nerve  cells  in  the  anterior  horns. 

The  rubrospinal  tract  (Monakow's  bundle  or  fasciculus  intermediolateralis).  From  the  nerve  cells  in 
the  red  nucleus  axons  descend,  after  decussation  in  the  tegmentum,  in  the  contralateral  side  of  the 
pons,  medulla  and  spinal  cord,  in  which  latter  they  lie  in  front  of  the  pyramidal  tract  and  hence  this  tract 
is  some  times  called  the  "pre-pyramidal   tract"    They  terminate  near  the  nerve  cells  in  the  anterior  horns. 

The  tectospinal  tract.  From  nerve  cells  in  the  corpora  quadrigemina  axons  descend,  decussate  beneath 
the  aquaeductus  Sylvii  and  pass  downward  through  the  formatio  reticularis  and  the  anterior  and  lateral  col- 
umns of  the  spinal  cord  to  the  nerve  cells  in  the  anterior  horns. 

The  vestibulospinal  or  Deiter's  tract.  From  nerve  cells  in  Deiter's  vestibular  nucleus  axons  pass  down- 
wards, mainly  without  decussating,  through  the  anterior  and  lateral  columns  of  the  spinal  cord  to  the  nerve 
cells  in  the  anterior  horns. 


The  ponto-spinal  tract.  From  cells  of  the  formatio  reticularis  axons  pass  in  part  directly  downwards  in 
the  lateral  column  of  the  same  and  of  the  opposite  side  of  the  cord  to  the  nerve  cells  in  the  anterior  horns. 

The  neurons  of  the  last  five  of  the  above  mentioned  tracts  constitute  the  extra-pyramidal  motor  tracts. 
They  all  terminate  in  the  nerve  cells  of  the  anterior  horns  and  have  to  do  with  automatic  and  associated  move- 
ments, and  muscle-tone.  Lesions  of  these  tracts  are  apt  to  cause  motor  disturbances,  such  as  tremor,  rigidity 
and  athetosis,  but  no  paralysis  of  voluntary  motion,  as  long   as   the   pyramidal   tract   is   normal. 

Between  these  bundles  of  centripetal  and  centrifugal  libers  and  connecting  the  former  with  the  latter  lie 
the  central  ganglionic  masses  of  the  spinal  cord  and  brain,  which  receive  the  impulses  coming  through  the 
centripetal  fibers  and  shunt  them  along  various  different  tracts  of  the  centrifugal  fibers,  producing  the  rel- 
atively simple  reactions  of  the  spinal  cord  and  the  extremely  complex  reactions  of  the  brain. 

Although  the  cortical  motor  centers  represent  almost  exclusively  muscles  lying  on  the  opposite  side  of 
the  body,  it  appears  from  clinical  observation  and  physiological  experiment  that  the  muscles  of  the  body  have 
a  bilateral  cortical  representation.  By  electrical  stimulation  of  the  cortex,  the  muscles  on  the  same  side  of  the 
body  may  be  made  to  contract ;  although  a  much  stronger  irritation  of  the  center  is  needed  than  is  necessary 
to  cause  a  contraction  of  the  corresponding  muscles  of  the  opposite  side  of  the  body.  Those  muscles  on  both 
sides  of  the  body  which  usually  act  together  (diaphragm,  etc.,)  have  especially  well  marked  bilateral  repre- 
sentation; so  that  these  muscles  are  rarely  completely  and  permanently  paralysed  in  unilateral  cerebral  lesions. 
A  cortical  paralysis  may  abolish  motion  only  and  may  be  very  circumscribed:  two  or  three  fingers,  or  the  thumb 
alone.  The  actions  which  are  especially  lost  in  the  cortical  lesions  are  the  purposeful  actions  which  have  been 
slowly  acquired  as  the  result  of  experience  and  training :  actions   which  are  peculiarly  voluntary  and  skillful. 

A  destructive  lesion  of  either  the  upper  or  the  lower  motor  neurons  will  cause  a  motor  paralysis.  If  the 
lower  motor  neurons  are  destroyed  there  will  be  a  paralysis  both  of  voluntary  and  of  reflex  acts:  a  flaccid 
paralysis  with  atrophied  and  degenerated  muscles  (252)  ;  while  if  the  upper  motor  neurons  are  destroyed  there 
will  be  a  spastic  paralysis  of  voluntary  acts  without  muscle  alterations ;  the  reflex  acts  persisting  and  being  in- 
creased:  a  spastic  paralysis  (251).  (For  explanation  of  the  increase  of  reflex  activity  just  mentioned,  see 
page  II). 

The  Sympathetic  System  is  not  considered  in  this  brief  review  of  the  physiology  of  the  nervous  system, 
because  the  Sympathetic  System,  important  as  it  is,  plays  little  part  in  the  diagnosis  of  nervous  diseases 
(Chart  XVIId). 

Movements  (Charts  IV,  V,  X) 

When  a  sensory  surface  is  irritated  the  animal  often  responds  immediately  by  a  comparatively 
simple  movement,  or  the  movement  may  occur  only  after  a  considerable  space  of  time  and  may  be 
very  complicated,  or  it  may  never  occur.  Movements  may  also  apparently  occur  spontaneously, 
not  being  preceded  by  any  sensory  irritation  in  the  immediate  past;  although  on  careful  analysis 
these  spontaneous  movements  can  always  be  referred  back,  indirectly,  to  some  sensory  irritation. 
All  the  actions  of  man  or  animal  (for  the  day  is  past  when  the  difference  between  man  and  ani- 
mals was  regarded  as  fundamental  and  not  merely  one  of  degree)  have  their  origin  immediately  or 
remotely  in  sensory  irritation  or  excitation,  and  all  these  different  kinds  of  movements  may  be  di- 
vided into  two  great  classes :  subcortical  and  cortical  reflexes,  according  as  the  neurons  concerned 
in  the  production  of  these  acts  have  their  cell  bodies  situated  in  the  gray  matter  of  the  spinal  cord 
and  basjd  ganglia  or  in  that  of  the  cortex  of  the  brain.  Automatic  acts  are  complicated  reflex  acts 
and  may  be  either  subcortical  or  cortical. 

Subcortical  Reflexes  and  Inhibition  (Chart  V) 

The  Simple  Reflex.  The  centripetal  nerve  fibers  terminate  in  the  gray  matter  of  the  spinal 
cord  and  in  that  of  the  brain  stem.  Some  of  the  nerve  fibers,  those  conducting  the  impressions  re- 
sulting from  tactile,  and  especially  those  from  painful,  stimuli,  terminate  in  synapsis  with  the  den- 
drons  of  nerve  cells  lying  in  the  posterior  horns  of  the  cord  or  in  the  sensory  nuclei  of  the  brain 
stem.  Through  these  latter,  the  impulse  is  transmitted  to  a  group  of  nerve  cells  in  the  anterior 
horns  of  the  spinal  cord  or  in  the  motor  nuclei  in  the  brain  stem  and  along  the  axons  of  these  lat- 
ter cells  to  the  muscles,  causing  tliem  to  contract  and  produce  a  motion  which  is  called  a  reflex 
act.  This  group  of  nerve  cells  innervates  not  one,  but  a  number,  of  muscles,  in 
varying  degree,  to  produce  a  definite  purposeful  movement  and  this  resulting  movement 
is  to  a  degree  orderly:  "coordinated."  The  nervous  complex  ju.st  described  may  occur  en- 
tirely through  one  segment,  or  metamere,  of  the  spinal  cord  and  is  called  the  "unconditioned  re- 
flex," t.  e.,  not  depending  on  other  complicating  factors  or  conditions.  It  is  so  simple  that  it  oc- 
curs very  rarely,  perhaps  never,  in  man ;  although  it  does  occur  in  all  its  simplicity  in  some  of  the 

10 


lower  animals.  It  occurs  in  frogs  and  most  clearly  in  those  whose  spinal  cord  has  been  separated 
from  the  brain  by  a  transverse  cut  at  any  point  above  the  reflex  arc  involved  in  the  act.  A  reflex 
act  is  a  reaction  from  an  irritation,  which  under  like  conditions  always  take  place  in  exactly  the 
same  way;  it  seems  purely  mechanical,  as  if  a  machine  were  working.  The  irritation  may  be  a 
usual  (normal  or  adequate),  or  unusual  (abnormal  or  inadequate)  one;  the  former  being  much 
more  effective ;  and  it  may  arise  from  stimulation  of  the  skin,  mucous  membrane,  muscle  tendon 
or  fascia,  or  of  any  of  the  organs  of  special  sense.  The  centripetal  neuron,  the  centrifugal  neuron 
and  the  connecting  neuron  joining  together  the  two  others  form  what  is  called  the  spinal  or,  in- 
cluding the  brain  stem,  the  subcortical  reflex  arc.  It  is  the  simplest  and  most  primitive  form  of 
nervous  reaction  and  is  the  type,  or  pattern,  of  all  other  more  complex  forms  of  nervous  reaction. 
For  its  production  there  is  necessary  a  receptor  (end-organ),  a  conductor  (neurons)  and  cm. 
effector  (muscle  or  gland).  By  the  neurons  the  receptor  and  the  effector  are  brought  into  inti- 
mate connection.  Usually,  if  not  always,  many  groups  of  nerve  cells  lying  in  different  levels  and 
the  coordinating  influence  of  the  cerebellum  take  part  in  the  ordinary  reflex  activity.  Such  simple 
reflex  acts  are  the  only  ones  occurring  in  the  body  during  the  early  months  of  life  and  are,  at  first, 
unconscious  acts,  and,  indeed,  many  reflex  acts  occur  unconsciously  throughout  life  (pupillary, 
etc.).  Similar  reflex  acts  cause  the  respiratory  and  cardiac  movements, the  flow  of  saliva  and  other 
secretions,  the  vascularity  of  organs  and  consequently  the  wannth  of  the  body,  and  in  general  regu- 
late the  physiological  actions  of  the  body.  These  are  called  instinctive  or  hereditary  actions;  the 
result  of  the  experience  of  ancestors  and,  therefore,  called  phylogenctic  in  contradistinction  to 
ontogenetic  acts,  which  are  acquired  by  the  education  and  experiences  of  the  individual.  Muscular 
tonicity  is  a  variety  of  reflex  action  and  disappears  in  destructive  lesions  of  anv  part  of  the  reflex 
arc  (240). 

The  groups  of  nerve  cells  lying  in  the  anterior  horns  and  causing,  when  in  activity,  a  definite 
coordinated  movement  are  called  "common  paths."  These  are  the  paths  by  which  nervous  impulses 
coming  from  different  parts  of  the  body  leave  the  spinal  cord  to  produce  the  reflex  act  and  are  the 
paths  which  all  these  nervous  impulses  have  in  common ;  while  the  sensory  impulse  arising  from 
irritation  of  any  one  sensory  surface  is  called  a  "private  path,"  and  is  at  the  service  of  only  one 
group  of  end-organs. 

The  reflex  act  is  influenced  by  many  other  conditions.  Slight  irritative  lesions  of  the  reflex  arc 
cause  exaggeration,  while  destructive  lesions  cause  abolition,  of  reflex  action.  If  the  neurons  in  the 
cord  are  excited  by  a  strong  painful  irritation  of  a  peripheral  nerve,  as  for  instance  the  bathing  of  a 
sciatic  nerve  of  the  frog  in  a  strong  salt  solution,  the  reflex  acts  will  not  take  place.  It  is  said  to  be 
inhibited.  It  can  also  be  inhibited  by  strong  impulses  coming  down  to  the  cord  from  the  higher 
nerve  centers.  Finally,  a  reflex  act  during  its  occurrence  inhibits,  more  or  less  completely,  all  other 
reflex  activity  of  the  spinal  cord,  and  especially  inhibits  the  activity  of  the  antagonistic  muscles. 

The  voluntary  abolition  of  reflex  activity  (inhibition)  may  be  brought  about  by  a  contraction 
of  those  muscles  which  antagonize  the  muscles  taking  part  in  the  reflex  act,  or  this  latter  act  may  be 
"inhibited"  by  a  direct  action  upon  the  subcortical  motor  cells  restraining  them  from  taking  part  in 
it,  nullifying  their  activity.  In  addition  to  this  voluntary  inhibition,  a  great  variety  of  nervous  ac- 
tivities taking  place  in  almost  any  part  of  the  nervous  system  (especially  strong,  painful  impres- 
sions), and  even  the  normal  process  of  cerebral  activity  will  cause  a  more  or  less  complete  inhibition 
of  reflex  activity  of  the  lower  parts  of  the  cord.  Complete  destruction  or  section  of  the  upper  part 
of  the  spinal  cord  is  said  to  abolish  all  reflexes  in  the  lower  part.  This  phenomenon,  if  it  really 
exists,  except  as  a  temporary  one  due  to  shock,  etc.,  has  not  been  satisfactorily  explained 
and  is  in  marked  contrast  to  the  exaggerated  reflexes  found  in  incompletely  destructive  lesions  of 
the  upper  portion  of  the  cord,  and  appears  from  the  most  recent  observations  to  have  no  founda- 
tion in  fact. 

Conduction  of  reflex  or  other  impulses  along  the  peripheral  nerves  is  equally  rapid  whatever 
may  be  the  intensity,  or  quality,  of  the  irritation,  but  conduction  through  the  gray  matter  is  much 
slower  and  varies  greatly  with  the  intensity  and  quality    of    the    irritation.     The    gray    matter  also 
possesses  the  power  of  summation ;  so  that  excitations  too   feeble  to  give  rise  to  a  reflex  may  be- 
ll 


come  potent  ones  by  repetition  at  very  short  intervals  of  time.  The  gray  matter  immediately  fol- 
lowing its  activity  shows  a  "refractory  period"  of  longer  or  shorter  time,  during  which  it  is  inexcit- 
able  or  exhausted.  This  indicates  that  the  gray  matter  accumulates  energy  during  rest,  which  it 
discharges  when  in  activity.  This  refractory  period  may  play  its  part  in  rhythmical  action ;  such 
as  the  heart-beat.  Most  reflex  acts  are  purposeful  and  healthful  in  their  nature.  Many  of  them  are 
absolutely  essential  for  life.  They  may  be  divided  into  the  offensive  and  defensive. 

A  destructive  lesion  of  any  pwrtion  of  the  reflex  arc  causes  abolition  of  the  reflex  acts,  as  does 
also  a  strong  irritation  of  tlie  higher  nerve  centers.  Slight  irritative  lesions,  such  as  slight  inflamma- 
tions, involving  any  portion  of  the  reflex  arc,  vnll  cause  an  exaggeration  of  the  reflex  act,  as  will 
also,  and  more  commonly,  a  lesion  which  interferes  with  conduction  of  nervous  impulses  (in- 
liibitory  impulses)  through  the  central  motor  (cortico-spinal)  neurons.  An  irritation, 
especially  a  continuous  one,  even  if  not  very  intense,  wrill  often  cause  a  tonic  spasm  or  contracture. 

Coordination   (43,  248,  638) 

The  centripetal  neurons,  which  enter  the  cord  through  the  posterior  horns,  in  part,  as  we  have 
just  described,  run  forward  and  passing  through  a  connecting  neuron  to  a  motor  neuron  in  the  an- 
terior horn  form  a  "reflex  arc."  Other  centripetal  neurons  run  upwards  in  the  spinal  cord  in  various 
tracts,  already  described  on  previous  pages,  to  the  higher  nervous  ganglia  lying  within  the  skull. 
Some  of  these  ascending  neurons  pass,  directly  or  indirectly,  to  the  cerebellum,  which  is  the  great 
coordinating  center  of  the  nervous  system.  As  we  have  learned,  the  simple  reflex  act  is  coor- 
dinated, a  number  of  muscles  being  concerned  in  the  act,  some  contracting  powerfully  and  others 
with  varying  degrees  of  intensity.  This  is  due  to  the  fact  that  the  nerve  cells  in  the  anterior  horns 
are  arranged  in  groups,  the  starting  point  of  the  "common  path;"  the  receptive  neuron  being  a 
"private  path."  Each  of  these  common  paths,  when  incited  to  action,  produces  a  definite  co- 
ordinated movement.  This  coordination  is  very  simple  and  applies  only  to  one  action.  Most  move- 
ments of  the  body  consist  not  of  one  but  of  a  series  of  coordinated  movements  in  definite  sequence. 
This  complicated  coordination,  both  for  reflex  and  for  so-called  voluntary  acts,  takes  place  in  the 
cerebellum  and  in  lesions  of  the  cerebellum  botli  these  kinds  of  actions  become  incoordinate,  ir- 
regular and  ineffective.  The  subcortical  reflex  is  congenitally  coordinated  (phylogenetic).  On 
the  other  hand,  coordination  due  to  cerebellar  influence  is  acquired  by  experience,  training, 
practice  (ontogenetic).  The  cerebellum  coordinates  a  series  of  reflex  acts  in  definite  coordinated 
succession. 

The  mechanism  of  the  action  of  the  cerebellum  is  very  little  understood.  As  already  described, 
the  centripetal  fibers  from  Flechsig's  tract  (the  direct  cerebellar  tract)  and  from  the  nuclei  of  the 
columns  of  Burdach  and  Goll  pass  through  the  restiform  bodies  to  the  Purkinje  cells  in  the  cere- 
bellar cortex.  From  the  semi-circular  canals,  through  the  vestibular  nerve,  fibers  run  to 
Deiter's  nucleus.  Centrifugal  fibers  run  from  the  dentate  nucleus  of  the  cerebellum 
to  the  red  nucleus  and  from  the  nucleus  and  from  Deiter's  nucleus  fibers  descend 
to  and  through  the  spinal  cord  in  tlie  extrapyramidal  tracts  already  mentioned. 
The  cortex  of  the  cerebellum  is  connected  with  the  cerebral  cortex  by  centripetal  fibers 
through  the  middle  peduncles.  Centripetal  fibers  also  run  from  the  dentate  nucleus  of  the 
cerebellum  to  the  red  nucleus  and  thence  to  the  cerebral  cortex  of  the  frontal  lobes  (the  cerebello- 
nibro-frontal  tract).  The  cerebellum  has,  therefore,  very  wide  connections.  From  recent  investiga- 
tions there  seem  to  be  definitely  localized  coordination  centers  in  the  cerebellar  cortex  similar  to 
those  long  since  demonstrated  to  exist  in  the  cerebral  cortex. 

The  Cortical  Reflexes 
In  addition  to  the  ascending  neurons  passing  to  the  cerebellum,  others  ascend  to  their  final 
termination  in  that  portion  of  the  cerebral  cortex  which  lies  posterior  to  the  fissure  of  Rolando, 
being  interrupted  in  their  course  by  various  ganglia  at  the  base  of  the  brain.  These  so-called 
"sensory  projection  fibers"  which  spring  from  definite  sensory  end-organs  terminate  in  definite 
and  distinct  cortical  areas.  Thus,  the  fibers  from  the  retina  (optic  fibers)  terminate  in  the  occi- 
pital lobe;  those  from  the  nose  (olfactory  fibers)and  those  from  the  mouth  (gustatory  fibers)  ter- 
minate in  the  cornu  Ammonis;  those  from  the  ear  (auditory  fibers)  terminate  in  the  anterior  trans- 

12 


verse  temporal  convolution,  those  from  the  skin  (tactile  fibers)  terminate  in  the  posterior  central 
convolution  and  those  from  the  muscles  (muscle  sense)  terminate  in  the  inferior  parietal  lobule. 
These  localized  areas  constitute  the  anatomical  basis  of  cerebral  localization  (Figs.  15  and  16). 
They  are  all  situated  in  the  hemisphere  contralateral  to  the  peripheral  sensory  organs  from  which 
their  long  projection  nerve  fibers  spring  (having  passed  through  sub-cortical  ganglia  in  their 
course).  These  areas  are  all  connected  together  by  nerve  fibers  (axons)  which  connect 
every  portion  of  the  sensory  cortex  with  every  other  portion.  These  are  called  "association 
fibers."  Finally,  from  each  of  these  localized  diflferentiated  sensory  areas,  bundles  of  axons 
pass  forwards  under  the  fissure  of  Rolando  to  the  anterior  central  convolution  and  its  immediate 
neighborhood  (the  so-called  motor  area  of  the  cortex)  and  come  in  contact  with  groups  of  neurons, 
the  axons  of  which  constitute  the  pyramidal  tract  and  terminate  in  those  groups  of  nerve  cells  in  the 
anterior  horns  of  the  cord  which  we  have  already  described  and  to  which  we  have  given  the  name 
of  the  common  path  along  which  impulses  pass  to  the  various  groups  of  muscles.  These  groups 
of  neurons  whose  cell  bodies  lie  in  the  anterior  central  convolution  (the  motor  area)  may  be 
called  the  common  path  for  the  impulses  coming  from  the  sensory  area  of  the  cerebral  cortex.  It 
is  quite  possible,  then,  for  a  nervous  impulse  entering  the  spinal  cord  through  a  posterior  nerve 
root,  not  only  to  pass  forward  to  the  motor  neurons  in  the  anterior  horns  and  produce  a  reflex  act, 
but  also  to  ascend  by  the  sensory  projection  fibers  to  the  cerebral  cortex  posterior  to  the  fissure  of 
Rolando  and  there  to  be  reflected  to  a  common  path  in  the  anterior  central  convolution  and  thence 
downwards  along  the  pyramidal  tract  to  the  same  common  path  in  the  anterior  horn  through 
which  the  spinal  reflex  impulse  passes. 

The  gray  matter  of  the  cord  is  compressed  into  the  center  of  the  cord,  of  which  it  forms  a  long 
continuous  "H"  shaped  axis.  Its  transverse  area  is  so  small  that  an  impulse  entering  through  the 
posterior  roots  finds  a  sliort  and  easy  route  to  the  common  path  and  passes  along  it  so  quickly  that 
it  is  not  apt  to  be  modified  or  inhibited  by  any  other  impulse  reaching  the  common  path  at  the  same 
instant.  Subcortical  reflexes  are,  therefore,  quickly  and  definitely  performed  and  are  relatively 
simple  in  character. 

The  gray  matter  of  the  cerebral  hemispheres,  on  the  other  hand,  is  not  compressed  into  their 
centers,  but  is  spread  out  in  a  large  area  over  their  entire  surfaces,  which  are  themselves,  greatly 
increased  in  extent  by  their  numerous  sulci.  When  an  impulse  reaches  the  cerebral  sensory  cortex 
through  the  sensory  projection  fibers,  it  may  pass,  as  we  have  said,  to  a  common  path  in  the  motor 
cortex.  It  may  also  pass  through  the  association  fibers  to  many,  widely  separated,  areas  of  the 
sensory  cortex  and  set  their  neurons  in  activity.  Through  these  latter  numerous  neurons,  impulses 
may  also  pass  to  the  same  common  path,  some  tending  to  increase,  others  to  impede  or  abolish,  its 
activity.  The  cortical  reflexes  are,  consequentiy,  slower  than  the  subcortical  and  do  not  follow 
immediately  up)on  the  excitation.  They  may,  indeed,  be  delayed  days,  weeks,  even  years  after  the 
time  of  the  original  excitation  which  was  the  primary  cause  of  them.  They  may  never  occur. 
They  may  be  exceedingly  characteristic  individual  acts  very  different  from  the  stereotyped  reflex 
acts  and  may  consist  of  a  great  variety  of  successive  acts. 

Just  as  the  subcortical  reflexes,  so  the  cortical  reflexes  have  been  the  object  of  much  experi- 
mental work.  One  of  the  earliest  of  these  recent  series  of  experiments  was  performed  by  Pav- 
low.  His  results,  stated  briefly  and  without  details,  are  that  the  salivary  secretion  of  a  dog, 
which  is  normally  caused  by  food  in  his  mouth,  can  be  excited,  after  a  course  of  training  or  edu- 
cation, by  optic  excitations  (one  of  various  colors  or  of  different  intensity  of  the  same  color),  or 
by  auditory  excitations  (one  of  various  sounds  or  different  intensities  of  the  same  sound),  with- 
out food  in  any  way  entering  into  this  final  acquired  reaction.  This  reaction  will  not  occur  if  the 
corresponding  sensory  cortical  area  be  destroyed.  A  very  slight  sensory  excitation  occurring  at  the 
same  time  will  abolish  or  impair  it.  It  is  a  cortical  reflex  but  has  in  large  degree  the  character- 
istics of  the  spinal  reflex.  It  is  called  the  "conditioned  reflex"  in  contradistinction  to  the  "uncon- 
ditioned" reflex :  the  normal  response  to  food.  The  conditioned  reflex  is  not  acquired  by  punish- 
ment and  reward,  but  merely  by  association  and,  when  acquired,  does  not  result  in  pleasure  or  pain. 
It  is  a  true  reflex  with  no  emotional  content. 

Somewhat  analogous  reflexes  (sometimes  called  motivated  reflexes)   have  been  acquired  by 

13 


animals  as  the  result  of  long  training  by  means  of  punishments  and  rewards:  such  as  rats  finding 
their  way  through  a  maze  and  the  training  of  animals  in  various  ways,  and  more  broadly  in 
"forcing  the  formation  of  sensory  habits."  Much  and  most  fruitful  work  has  been  done  in  this 
line.  The  human  being  undergoes  a  very  similar  training,  directed  by  rewards  and  punishments, 
in  the  home,  the  school  and  in  life. 

The  cortical  reflexes,  often  called  the  "association  reflexes,"  and  known  by  a  still  older 
designation,  "voluntary  movements,"  are  the  result  of  education.  Given  the  knowledge  of  a  per- 
son's education,  and  enviroment  in  all  its  details,  his  acts  can  be  predicted  with  a  great  deal  of 
certainty  and  are  practically  so  predicted  by  his  fellow  men,  even  though  they  do  not  know  all  the 
details  of  his  heredity,  which  knowledge  is,  of  course,  also  necessary  for  an  infallible  judgment. 
(See  voluntary  movements.) 

The  subcortical  reflexes,  the  simple  reflex  acts,  may  be  entirely  unconscious  ones.  They  are 
most  marked  when  by  a  lesion  the  spinal  cord  in  its  entirety  or  its  lower  portion  is  separated  from 
the  brain,  and  in  such  cases  (which  are  of  not  infrequent  occurrence)  the  individual  has  no  con- 
sciousness of  the  movements  of  his  arms,  or  legs  or  sphincters,  unless  he  is  looking  at  them. 

The  cortical  reflexes,  on  the  other  hand,  are  usually  associated  with  very  remarkable 
phenomena  (including  consciousness),  which  we  have  next  to  discuss. 

Before  doing  so  it  may  be  noted,  as  a  summary  of  previous  statements,  that  there  are  three 
ways,  and  only  three,  in  which  an  animal  responds  to  the  various  stimuli  coming  from  the  external 
world : 

1st.  Reflex  Acts  which  are  centered  in  the  spinal  cord  and  brain  stem,  and  which  are 
relatively  slightly,  or  not  at  all,  modified  by  other  stimuli. 

2nd.  Automatic  Acts,  centered  in  the  corpus  striatum  and  nucleus  lenticularis  and  greatly 
modified  by  other  stimuli  including  the  emotions. 

3rd.  Volutary  Acts,  centered  in  the  cerebral  ■  cortex  and  profoundly  modified  by  many  stimuli 
arising  from  present  and  past  perceptions,  matured  judgments,  habits  and  emotions. 

The  "So-called"  Psychic  Functions  (Charts  III  and  XVI) 

So  far  in  our  discussion  of  cerebral  activity  (the  excitation  of  the  sensory  cortex  and  the  con- 
ditioned, motivated  and  associated  reflexes  which  result),  we  have  been  dealing  with  facts  which 
can  be  definitely  proved  by  anatomical  and  physiological  investigation.  What  we  have  considered 
however,  does  not,  by  any  means,  include  all  the  phenomena  connected  with  cerebral  activity. 

When  a  nervous  impulse  reaches  the  sensory  cortical  area  it  produces,  if  of  sufficient  inten- 
sity, a  phenomenon  called  sensation.  Thus,  when  we  are  looking  at  a  tree  we  appreciate  something 
which  we  call  the  sensation  of  the  sight  of  a  tree.  It  is  often  called  the  image  of  a  tree  although 
there  is  in  the  brain  nothing  like  an  image  on  a  photograpliic  plate  of  the  tree,  but  rather  a  cor- 
tical activity  which  is  the  symbol  of  a  tree.  Moreover,  while  we  are  looking  at  the  tree,  there  is  tak- 
ing place  another  cerebral  activity  of  which  we  are  entirely  ignorant  and  unconscious — a  permanent 
change  occurs,  whether  static  or  dynamic,  which  constitutes  a  memory  of  the  tree;  so  that  when 
we  close  our  eyes  an  image  of  the  tree  may  remain,  which  we  clearly  see  and  which  is  perfectly 
true;  although  it  does  not  possess  the  quality  of  reality.  This  memory  of  this  identical  tree  re- 
mains permanently  in  the  brain,  potentially,  and  can  at  any  time  be  brought  into  consciousness 
(a  term  later  to  be  defined)  by  a  process  which  is  called  the  as.sociation  of  ideas  (also  later  to  be 
defined). 

Sensation  and  memory  are  the  basic  factors  in  psychology  and  upon  them  is  built  up  the 
elaborate  structure  of  this  science,  whether  it  be  called  introspective  or  phy.siological  psychology. 
Sensation  undoubtedly  is  a  manifestation  of  force,  the  product  of  the  oxidation  of  the  nutriment 
in  the  blood  and  ceases  as  soon  as  the  blood  ceases  to  flow  in  the  corresponding  part  of  the  cerebral 
cortex,  but  no  psychologist  or  physiologist  has  ever  satisfactorily,  or  even  intelligibly,  defined  what 
sensation  really  is.  This  is  true  of  many  of  the  other  natural  forces.  To  mention  only  two: 
gravitation  and  electricity  have  never  been  explained.  Their  essential  nature,  after  centuries  of 
observations,  is  not  yet  understood.     This  does  not  prevent  our  studying  them  and  discovering 

14 


that  they  invariably  act  in  certain  well  defined  ways,  tliat  they  follow  certain  laws ;  and  by  avail- 
ing ourselves  of  our  knowledge  of  these  laws  these  forces  have  become  our  very  useful  slaves.  It 
may  be  that  in  the  future  we  shall  discover  the  essential  nature  of  these  forces  more  or  less  com- 
pletely, but  that  day  is  not  yet.  We  may  also  discover  what  sensation  is,  but  it  can  even  now  be 
studied,  and  as  a  matter  of  fact  this  form  of  energy  is  being  experimented  with  in  every  psycho- 
logical and  physiological  laboratory  in  the  land. 

The  Psychology  handed  down  to  us  by  our  fathers  attempts  to  solve  these  facts  by  traditional 
authority,  by  abstract  reason  and  by  introspection  and  has  introduced  the  element  of  the  super- 
natural and  of  mystery.  The  result  after  thousands  of  years  of  this  study  has  been  far  from 
satisfactory.  Our  knowledge  acquired  by  these  means  has  advanced  little,  if  at  all,  beyond  that 
of  the  ancient  Grecian  philosophers.  To  the  physiological  psychologist  of  recent  years  these  facts 
still  await  solution ;  but  to  him  they  are  the  result  of  cortical  activity  and  do  not  require,  and  prob- 
ably will  never  require,  a  supernatural  explanation.  What  sensation  is,  has  not  been  explained 
either  by  the  scientist  or  by  the  philosopher.  To  the  former,  however,  it  appears  to  be  energy  pro- 
duced by  cortical  activity. 

The  mystery  of  the  mechanism  of  the  animal  body  is  beirig  slowly  dispelled  by  investigation. 
This  investigation  has  been  carried  on,  and  is  being  carried  on,  under  many  difficulties.  The  dis- 
section of  the  human  body  and  experimentation  on  animals  is  still  repugnant  to  many.  The  prej- 
udices of  mankind  have  to  be  reckoned  with.  Many  higlily  educated  men,  while  granting  that 
most  of  the  organs  of  the  human  body  are  in  their  activity  subject  to  ordinary  physical  laws  and 
that  the  source  of  their  activity  is  the  nutriment  in  their  blood  supply,  are,  yet,  unwilling  to  grant 
that  the  activity  of  the  nervous  system  is  to  be  explained  in  the  same  way.  They  point  out  that 
most  of  the  internal  organs  take  certain  chemical  substances  from  the  blood  and  convert  them  only 
into  other  chemical  substances  and  that  the  chemist  in  his  test  tubes  and  other  apparatus  can  imitate 
these  reactions  more  or  less  perfectly.  They  omit  to  state,  however,  that  there  is  one  set  of  organs, 
the  muscular  system,  much  more  extensive  than  any  other  organs  in  the  body,  which  takes  the 
nutriment  from  the  blood  and  transmutes  it  into  a  form  of  energy,  contractility,  and,  thus,  does 
exactly  what  the  nervous  system  does,  when  it  transmutes  the  nutriment  in  the  blood  into  forms 
of  energy  called  the  sensation,  consciousness,  etc.  The  reason  that  I  am  devoting  what  may  appear 
to  be  too  much  space  to  this  subject  is  that  I  am  desirous  of  presenting  the  physiology  of  the  nerv- 
ous system  on  a  physiological  rather  than  on  a  mystical  basis;  and,  yet,  what  is  here  presented  is 
but  a  bare  outline  of  the  subject  and  is  in  need  of  much  amphfication. 

Sensation  and  consciousness,  whatever  their  nature  may  be.  are  the  fundamental  elements  m 
any  aspect  of  psychology  or  of  cerebral  physiology,  if,  indeed,  any  distinction  can  be  drawn  be- 
tween these  two  sciences.  They  are  the  "Axiom"  or  the  "Given"  of  mathematics,  of  logic  and  of 
psychology.     They  are   self-evident   propositions  which  cannot  be  further  analysed. 

Sens.\tion  (Ch.\rts  VI  and  XIV) 

When  the  various  impulses  originating  in  the  sensory  end-organs  have  passed  along  the 
various  tracts  and  have  traversed,  and  been  interrupted  by,  several  masses  of  gray  matter,  they 
reach  the  sensory  area  of  the  cerebral  cortex  and  there  give  rise  to  a  new  form  of  energy  called 
sensation.  That  is  to  say,  a  physical  force  (as  for  instance,  ether  in  rapid  undulation)  is  con- 
verted in  a  terminal  organ  into  nervous  energy,  and  as  such,  having  traversed  the  sensory  tracts, 
reaches  the  cerebral  cortex.  It  is  there  transmuted  into  a  new  form  of  energy  (as  for  instance 
the  sensation  of  light).  The  sensation  of  light  takes  place  in  the  brain,  not  in  the  eye,  and  has 
no  similarity  to  the  undulations  of  ether  from  which  it  normally  originates,  and  it  may,  indeed,  be 
caused  not  only  by  these,  but  also  may  originate,  in  perfect  darkness,  from  mechanical  irritation  of 
the  eye  (as  by  pressure  from  the  finger  upon  the  eyeball)  or  of  the  optic  nerve.  Sensation 
is,  therefore,  rather  a  symbol  than  a  picture  (the  image  of  the  older  psychology)  of  the  external  ob- 
ject, with  wliich  by  experience  it  is  associated. 

Sensation  is  thus  a  special,  individual  form  of  energy,  similar  to  electricity,  hght,  etc.,  which 
is  produced  in  the  cerebral  cortex  and  which  has  its  special   individual  characteristics.     It  has  an 

15 


analogy  to  electricity  produced  on  amber  by  friction.  Sensations  originating  from  the  different 
organs  of  sense  are  located,  as  we  have  seen,  in  different  and  special  portions  of  the  cortex  (Figs. 
15  and  16)  and  do  not  at  all  resemble  the  external  phenomena  causing  them.  A  clap  of  thunder 
and  a  flash  of  lightning  are  very  different  external  phenomena,  but  the  reactions  in  the  cortex, 
which  constitute  these  sensations,  probably  \^ry  in  topography  rather  than  in  quality.  We  know 
nothing  more  of  the  essence  of  this  form  of  energy,  which  we  call  sensation,  than  we  do  of  the 
essential  nature  of  electricity,  or  of  contractility  in  the  muscle  fiber  or  in  the  amoeba.  We  know 
something  of  its  effects  and  we  know  something  of  the  locality  of  the  cerebral  cortex  in  which  it 
occurs  (Figs.  15  and  16)  and  that  it  is  very  dependent  upon  abundant  blood  supply  and  we  believe 
that  it  depends  upon  physico-chemical  actions  taking  place  in  the  cortex.  Conscious  sensation, 
probably,  occurs  only  in  those  animals  which  possess  cerebral  hemispheres. 

Sensation  and  all  other  forms  of  mental  activity  are  absolutely  dependent  upon  a  fairly 
healthy  cerebral  cortex  and  a  fairly  abundant  blood  supply  to  it.  When  the  cerebral  hemi- 
spheres in  an  animal  are  removed,  or  when  the  cerebral  cortex  in  man  is  entirely,  or  mainly,  de- 
stroyed by  disease,  or  in  a  child  the  hemispheres  are  absent  or  very  defective,  or  when  the  blood 
supply  is  cut  off  from  the  cerebral  cortex  altogether  or  in  large  part,  then  sensation,  perception, 
memory,  thought,  emotion  (and  its  corporeal  expression,  except  in  anger),  ethics,  association  of 
ideas,  voluntary'  motion,  inhibition,  intelligence,  personality  and  consciousness  are  all  lost. 

Sensation  is  the  simplest  manifestation  of  consciousness  (see  later)  or  cognition.  For  its 
production  a  certain  degree  of  intensity  of  the  nervous  impulses  is  essential  (the  threshold),  below 
this  point  of  intensity  the  cortex  may  be  in  activity,  but  sensation  will  not  result;  the  activity  vrill 
be  subconscious.  A  series  of  slight  subliminal  impulses.  o,uickly  repeated,  may  by  summation 
cause  sensation.  There  is,  therefore,  a  minimum  of  intensity  necessary  for  sensation ;  just  as 
electricity  passing  through  a  wire  must  have  a  certain  intensity  before  the  wire  glows  and  light  is 
produced.  There  is  also  a  maximum  beyond  which,  no  matter  how  great  the  irritation,  there  is 
no  increase  of  sensation,  but  rather  a  diminution  from  exhaustion  of  the  nerve  cells.  Between 
this  minimum  and  maximum  point,  sensibility  increases,  or  diminishes,  not  continuously,  but 
by  little  steps :  a  definite  ratio  to  the  stimulus,  in  accordance  with  Weber's  law,  which,  although 
not  absolutely,  is  approximately,  correct,  especial'y  for  stimuli  of  moderate  intensity. 

Furthermore,  a  weak  or  moderately  strong  excitation  may  reach  the  cortex  at  a  time  when  other 
portions  of  the  cortex  are  in  such  strong  excitation  that  this  weak  irritation  may  produce  no  sen- 
sation, but  remains  subconscious,  is  inhibited  by  the  stronger  cortical  activity.  The  line  between 
the  con5^ious  and  the  subconscious  cannot  be  sharplv  drawn.  Subconscious  cerebral  activity 
is  much  greater  in  volume,  although  much  less  in  intensity,  than  is  cerebral  activity  resulting  in 
consciousness.  Scnsatior  is  the  intcr-reaction  between  a  relatively  strong  nervous  impulse  from 
an  organ  of  sense  and  f'' •  cortical  activities  constituting  the  memories  of  those  previous  perceptions, 
emotions,  etc.,  which  rr-  the  individual's  personality. 

Perceptions  and  Concepts   (Chart  VI). 

A  perception  consists  of  a  combination  of  sensations,  which  are  obtained  from  various  sensory 
end-organs,  all  of  which  proceed,  usually  simultaneously,  from  the  same  external  object.  A  percep- 
tion of  an  apple  is  composed  of  several  sen.sory  impulses:  of  visual  sensations  caused  by  nervous 
impulses  from  the  retina,  representing  the  outline  and  markings  and  color  of  the  apple;  of  muscle 
sensation  caused  by  nervous  impulses  from  the  ocular  muscles,  representing  its  distance  from 
the  eye,  its  position  in  relation  to  other  objects  and  to  some  extent  its  form;  of  tactile  sensations 
cau.sed  by  nervous  impulses  from  the  hand,  representing  its  form,  firmness  and  texture ;  and  of 
gustatory  sensations  caused  by  nervous  impulses  from  the  mouth,  representing  its  taste.  The 
various  physico-chemical  changes,  thus  set  in  activity  in  the  cortex,  combine  to  produce  the  full 
perception  of  the  apple,  which  perception  is  greatly  modified  by  our  emotions,  moods,  memories 
and  the  then  present  other  perceptions,  and  is  not  exactly  the  same,  sometimes  widely  different,  in 
different  men.  The  perception  of  an  apple  by  Adam  was  probably  very  different  after  the  fall 
of  man  than  before  it.  For  a  full  and  complete  perception,  consisting  as  it  does  of  so  many  ele- 
mentary sensations,  quite  an  appreciable  time,  or  frequent  repetition,  is  needed.     It  is  quite  pos- 

16 


sible  that  a  full  perception  may  consist  both  of  conscious  and  subconscious  elements.  The 
kinesthetic  sense,  for  instance,  is  rarely,  if  ever  a  conscious  sensation.  The  development  of  a 
perception  is  found  by  experiment  to  proceed  from  generalities  to  details.  A  combination  of  the 
full  perceptions  of  many  apples,  each  resembling  and  at  the  same  time  in  some  respects  differing 
from  the  others,  produces  the  idea  or  concept  of  an  apple,  with  which  is  associated  its  written  or 
spoken  name  and  any  other  experiences  or  knowledge  which  have  become  associated  during  our 
life  with  apples.     (See  also  under  Association.)     A  concept  is,  therefore,  an  abstraction. 

Perceptions  occur  in  the  cerebral  cortex  in  immediate  proximity  to  the  cortical  termination 
of  the  corresponding  projection  fibers.  Each  cortical  center  consists  of  a  smaller  portion,  in  which 
the  projection  fibers  terminate,  and  a  larger  portion,  in  which  perceptions  take  place 
and  in  which  their  memories  are  stored.  Thus,  the  optic  fibers  terminate  in  the 
lips  of  the  calcarine  fissure,  while  the  rest  of  the  median  and  convex  surface  of  the 
occipital  lobe  is  devoted  to  optic  perceptions  and  memories  (Figs.  15  and  16).  When 
sensations  only,  but  not  perceptions,  can  occur,  as  when  that  portion  of  the  center  in 
which  the  projection  fibers  do  not  terminate  is  diseased,  the  condition  is  called,  in  general,  agnosia. 
When  there  is  a  failure  of  tactile  perceptions  the  condition  is  called  astereognosis;  in  failure  of 
optic  perceptions,  soiil-Uindness,  or  psychic  blindness,  and  in  failure  of  auditory  perceptions,  sotiU 
deafness,  or  psychic  deafness,  or  auditory  or  sensory  apliasia.  When  that  portion  of  any  sensory 
area  of  the  cortex  in  which  the  sensory  fibers  terminate  is  diseased,  both  perception  and  sensation 
are  abolished. 

Memory  (Chart  III) 

When  perception  takes  place,  physico-chemical  changes  are  occurring  in  a  definite  portion 
of  the  cerebral  cortex,  which  not  only  produce  the  perception,  but  also  leave,  thereafter,  a  perma- 
nent alteration  in  the  cortex  (a  vestige).  The  energy  derived  from  the  chemical  changes  taking 
place  in  the  cortex  during  an  active  perception  may  result  in  a  structural,  physical  or  chemica] 
change  in  the  nervous  elements,  or  more  likely  in  the  storing  in  them  of  potential  energy,  which 
can  be  liberated  and  become  actual  later.  Memories  seem  to  be  dynamic  changes  in  nerve 
cells  and  fibers  which  reduce  the  resistance  to  subsequent  similar  impressions  or  excitations.  Cer- 
tainly, a  definite  change  is  brought  about  which  registers  a  permanent  memory  of  the  object  per- 
ceived and  subsequently  this  memory  can  be  latent  or  active  from  time  to  time.  Consciousness, 
the  actual  perception  of  an  object  and  its  associated  active  memories  (active  attention),  is  a  very 
exhausting,  energy  consuming  process  for  the  cerebral  cortex.  Subconsciousness,  and  the  pres- 
ervation of  memories,  not  actually  present  in  consciousness,  are  not  exhausting  to  the  cortex, 
even  though  the  memories  be  preserved  for  many  years. 

In  virtue  of  this  change  in  the  cortex,  a  memory  of  the  corresponding  object  always  results 
from  excitation  of  this  altered  cortex.  The  memory  may  be  aroused,  or  enter  into  cog- 
nition, by  the  external  force  which  originally  caused  it  and,  then,  the  object  will  be  recognized 
(re-known),  because  the  actual  perception  .corresponds  perfectly  vnth  its  memory; 
or  the  memory  may  be  aroused  by  way  of  association  fibers  which  the  original  perception  had 
previously  set  into  activity.  Memories  become  associated  with  each  other  in  accordance  with  the 
relationship  of  the  objects  causing  them,  as  the  result  of  our  experiences  with  these  objects.  In 
perception,  then,  a  trace  of  the  cortical  excitation  remains  in  the  cerebral  cortex  as  a  memory,  in 
a  sense  analogous  to  the  persistence  of  the  after-image  in  the  retina  after  strong  excitation  (look- 
ing for  some  time  at  a  bright  light).  The  retention  of  any  memory  depends  upon  the  frequency  of 
he  perception  causing  it,  its  interest  and  its  startling  nature.  The  recall  of  a  memory  is  by  ^vay 
of  the  association  fibers  from  a  perception  or  some  other  memory  associated  with  it. 

In  comparing  an  actual  perception  of  an  object,  or  an  experience,  with  its  memory,  if  the  two 
exactly  coincide  and  resemble  each  other,  there  is  not  only  the  act  of  recognition,  but  also  what  is 
called  "identification"  and  "similarity;"  whereas  if  the  perception  and  the  memory  of  a  former  per- 
ception do  not  exactly  coincide,  there  is  what  is  called  "non-identity"  and  "dissimilarity,"  and 
this  action  is  called  "discrimination."  This  cerebral  activity  with  its  two  results:  identification  or 
discrimination,  is  the  basis  of  classification,  systematizing  and  iudgment. 

17 


Memories  are,  however,  very  different  qualitatively  from  the  original  perceptions.  The  for- 
mer have  no  actuahty.  Even  though  they  may  be  at  times  very  vivid,  they  never  seem  real  to  a 
normal  personality.  This  is  due  to  the  absence  of  any  nervous  impulses  coming  simultaneously 
from  the  peripheral  sense  organ, especially  from  its  musculature,  which  were  present  in  the  original 
perception.  They  are  never  so  intense  as  the  original  perception.  It  is  almost,  if  not  quite 
impossible  to  recall  a  memory  derived  from  any  peripheral  organ  of  sense,  while  that  organ  is 
engaged  in  producing  an  actual  perception ;  the  actual  perception  is  much  too  strong  for  the  mem- 
ory and  the  latter  is  inhibited  l)y  the  former. 

The  cortex  of  the  brain  is  in  great  part  a  huge  store-house  of  memories.  The  memories  of 
any  object  vary  in  different  men  according  to  their  training,  education,  attention  and  former  asso- 
ciations with  the  object.  These  memories  are  grouped  together ;  so  that  those  which  are  derived 
from  the  same  organ  of  sense  lie  together  in  the  cortex.  This  localization  of  memories  has  been 
worked  out  with  great  care  and  is  to  a  considerable  extent  known.  It  is  shown  in  figures  15  and  16. 
A  local  cortical  lesion  may  thus  produce  a  loss  of  a  group  of  allied  memories. 

All  memories  are  sensory  in  character  with  the  excephon  of  one  extremely  doubtful  group. 
This  group  consists  of  memories  of  so-called  "innervation  feelings."  When  a  muscle  is  con- 
tracted the  person  to  whom  it  belongs  has  a  feeling  of  this  contraction  and  can  estimate  its  strength. 
Such  innervation  feelings,  if  existent,  are  sensory,  but  it  is  difHcult  to  be  conscious 
of    them.      They   are,    in    the   main,  subconscious.  This      feeling     is     called     an      "innerva- 

tion feeling''  and  its  memory,  it  is  claimed  by  some  investigators,  is  stored  away 
in  the  cortex  of  the  anterior  central  convolution  and  especially  in  the  neighborhood  in 
front  of  it.  This  innervation  feeling,  it  is  claimed,  is  essential  for  the  voluntary  performance  of  the 
corresponding  act.  When,  in  consequence  of  a  cortical  brain  lesion  in  the  area  in  which  these 
memories  are  stored,  a  person  loses  the  power  of  performing  certain  acts,  he  often  says,  "I  have 
forgotten  how  to  do  it."  These  innervation  feelings  and  memories,  if  they  really  exist,  do  not 
obtrude  themselves  strongly  into  our  consciousness.  They  have  rather  to  be  sought  for.  It  is, 
indeed,  very  difficult  if  not  impossible  to  be  conscious  of  them.  They  may,  however,  be  subcon- 
scious and  play  their  part  in  the  production  of  complex  perceptions. 

There  are  many  physiologists  and  psychologists,  however,  who  question  whether  there  are  any 
so-called  innervation  felings  or  memories,  and  regard  the  cortical  motor  cells  as  merely  "common 
paths"  similar  to  those  in  the  spinal  cord.  However  that  may  be,  whether  true  innervation 
memories  exist  or  not,  the  function  of  this  cortical  area  is  an  actuality  and  whenever  a  portion  of 
the  motor  cortex  is  sufficiently  excited  by  a  cellular  activity,  a  perception,  or  a  memory,  in  the  sen- 
sory cortex  so-called  voluntary,  or  association,  action   results.      (See   Voluntary   Movements). 

CoNSCrOUSNESS     AND     SUBCONSCIOUSNESS    (ChaRTS   III    AND    IV) 

Con.sciou.sness  and  subconsciousness  are  terms  used  to  express  the  fact  that  the  cerebral  cor- 
tex is  in  activity.  Although  convenient  expressions,  they  should  not  be  regarded  as  representing 
di.stinct,  possibly  conflicting,  entities.  They  are  both  component  parts  of  the  personality.  The 
difference  between  them  is  only  one  of  degree:  the  degree  of  intensity  of  the  local  cortical  activity 
which  produces  them  combined,  perhaps,  with  a  sense  of  "friction"  which  the  intense  activity 
meets  in  passing  through  the  cortical  neurons.  .A.s  this  resistance  decreases  with  repeated  use  an 
act,  at  first  conscious,  may  become  .subconscious.  A  person  is  at  times  unconscious  of  his  habits : 
his  habitual  acts.  .\t  one  instant  a  sen.sation,  a  perception,  a  concept,  an  idea,  a  thought,  a 
judgment  or  some  other  product  of  cerebral  activity  is  present  in  consciousness  becau.se  of  a  strong 
local  cortical  activity  and  the  next  instant  the  activity  becomes  less,  is  replaced  by  another  strong 
local  cortical  activity,  and  the  former  ceases  to  be  present  in  consciousness  and  becomes  a  part  of 
the  subconscious  cerebral  activity.  There  is,  thus,  a  constant  interchange  between  local  corti- 
cal activities  and  consequently  the  content  of  consciousness  is  constantly  changing.  The  fact  tliat 
an  intense  cortical  activity  makes  its  resulting  energy  an  integral  part  of  consciousness,  makes  it 
al.so  a  dominant  factor  in  any  judgment  or  action  which  may  result.  Normally,  during  life,  there 
is  constant  cortical  activity,  whether  it  is  an  activity  resulting  in  consciousness  or  subconscious- 
ness.    Furthermore,  there  are  all  degrees  of  intensity  of  this  activity  and  consequently  varying  de- 

18 


grees  of  consciousness  from  vivid  expectant  attention  (concentration),  to  passive  attention  (rev- 
erie) to  semiconsciousness,  to  stupor,  to  dreams  (by  night  or  by  day),  to  subconsciousness  and, 
in  the  absence  of  all  cortical  activity,  to  unconsciousness.  What  consciousness  really  is  we  know 
no  more  than  we  know  what  it  is  which  is  exhibited  by  amber  when  it  is  electrified  by  friction. 
Yet  we  do  not  hesitate  to  say  that  electricity  is  a  form  of  energy,  or  force,  produced  by  friction 
upon  amber,  by  a  dynamo,  or  by  numerous  other  means ;  and  just  as  we  say  that  the  potential 
energy  of  coal  may  be  converted  into  electricity ;  so  we  may  say  that  the  potential  energy  in  the 
blood  (derived  from  food)  is  converted  in  the  cerebral  cortex  into  conscious  sensations,  percep- 
tions, etc.,  or,  taken  collectively,  into  consciousness. 

Consciousness  consists,  at  any  instant  of  time,  of  the  then  present  perceptions  and  of  those 
past  memories  wliich  are  directly  or  indirectly  associated  with  these  present  perceptions  and  which 
have  been  awakened  by  them  into  activity  at  that  instant  of  time.  Consciousness  is  thus  a  form  of 
energy  resulting  from  a  high  grade  of  activity  of  the  cerebral  cortex.  The  other  memories,  at  that 
instant  active,  but  not  active  with  sufficient  intensity  to  enter  into  consciousness,  constitute 
subconsciousness  and  may  at  any  time  become  conscious  memories.  The  content  of  consciousness 
embraces  only  a  small  fraction  of  those  activities  which  take  place  in  the  brain  and  indeed  only  a 
fraction  of  those  activities  which  take  place  in  the  cerebral  cortex  at  any  instant  of  time. 

The  cortical  activities  constituting  consciousness  are  very  much  less  numerous  and  extensive 
than  those  constituting  subconsciousness.  When  we  first  dress  each  morning,  we  are  conscious  of 
the  contact  of  our  clothes  with  our  skin,  but  soon  this  sensation  ceases,  is  replaced  by  others  and  the 
cortical  activity  caused  by  the  contact  of  the  clothes  becomes  subconsciousness.  It  still  persists, 
however,  and  if  by  way  of  association  fibers  its  activity  be  slightly  increased  it  will  again  enter  con- 
sciousness and  the  sensation  will  again  arise  temporarily.  We  walk  in  the  street  and  are  conscious 
of  seeing  and  hearing  many  things,  but  many  other  things  cause  cortical  activity  of  such  low  in- 
tensity that  we  fail  to  be  conscious  of  them.  They  remain  subconscious  and  a  faint  memory 
of  them  persists  which  may  later  be  brought  into  consciousness  by  way  of  the  association  fibers,  the 
impulses  from  wliich  may  increase  the  subconscious  activity  to  a  degree  which  constitutes  con- 
sciousness. A  familiar  example  is  that  of  a  man  whose  attention  is  so  fully  occupied  that  he  does 
not  hear  the  striking  of  a  clock,  but  later  recalls  the  memory  of  this  sound,  which  memory  was  ob- 
tained subconsciously. 

Consciousness  and  personality  can  probably  be  best  studied  in  their  forming  in  infancy,  and  in 
such  a  study  they  may  well  be  found  to  consist  essentially  in  the  action  and  interaction  of  each 
new  perception  on  the  few  other  perceptions  previously  acquired,  which  at  that  date  constitute  the 
rudimentary  personality  of  the  child. 

A  new  born  babe  has,  probably,  no  consciousness.  An  infant  attains  consciousness  slowly  as 
he  gradually  obtains  perceptions  and  memories  and  forms  a  large  number  of  associations  of  all 
kinds.  When  an  infant  has  his  first  perception  this  one  percption,  together  with  certain  rudi- 
mentary sensations  he  may  have  acquired,  constitutes  his  entire  consciousness  and  his  entire  in- 
telligence. It  is  all  he  knows.  As  other  perceptions  are  obtained  and  associated 
together  his  intelligence  and  his  consciousness  become  larger,  more  distinct  and 
more  complete.  The  child  in  his  development  increases  with  great  rapidity  the  num- 
ber of  his  perceptions,  less  rapidly  and  subject  to  many  subsequent  corrections 
his  associations,  still  less  rapidly  his  concepts,  even  more  slowly  his  ethical  and  aesthetical 
ideas,  and  yet  more  slowly  his  abstractions.  But  at  the  end  of  a  few  years  any  perception  or 
memory  suggesting  action  is  subjected  to  the  interplay  of  all  these  activities  before  the  action  is  done 
or  left  undone.  In  other  words,  consciousness  and  the  act  of  thinking  and  reasoning  on  which 
action  is  based  (see  Voluntary  Motion)  are  already,  even  in  cliildhood,  very  complicated,  perhaps 
more  so  than  in  later  life,  when  action  is  mainly  determined  by  habits  of  thought  and  by  judg- 
ments firmly  established  by  numerous  experiences. 

Consciousness  is  a  form  of  energy,  such  as  light  and  electricity,  ivhich  is  transmuted  from  other 
forms  of  energy  by  physico-chemical  action  taking  place  in  the  cerebral  cortex.  Consciousness 
embraces  all  those  chemical  activities  which  have  a  certain  intensity;  below  this  degree  of  inten- 
sity the  activities  constitute  subconsciousness.     The  process  is  somewhat  analogous  to  that  in  an 

19 


electric  light  btilb  through  which  an  electric  current    may    be    constantly  flowing,  but  which  only 
gives  forth  light  when  the  current  has  attained  a  centain  intensity. 

Consciousness  is  constantly  being  newly  formed  and  is  dependent  upon  the  perceptions, 
memories,  feelings  and  ideas,  ethical  and  others,  present  at  any  one  instant.  These  phenomena 
themselves  constitute  and  are  consciousness.  None  of  them,  usually,  continues.  Others  are  con- 
stantly replacing  them.  None  remains  constant.  The  continuity  of  consciousness  is  preserved 
by  the  mingling  of  memories  of  past  perceptions  with  present  ones,  and  by  memories  of  past 
states  of  consciousness. 

Consciousness  has  narrow  limits.  It  cannot  contain  many  perceptions,  ideas,  etc.,  at  the  same 
time.  We  daily  take  advantage  of  this.  When  a  child  or  an  adult  is  conscious  of  a  painful  per- 
ception or  idea  and  is  consequently  unhappy  we  suggest  to  him  another  perception  or  idea  and 
emphasize  it  until  it  replaces  the  painful  one,  which  sinks  into  subconsciousness  and  is  less  domi- 
nant. 

Just  as  reflex  action  taking  place  in  the  spinal  cord  temporarily  inhibits  more  or  less  completely 
the  activity  of  the  rest  of  the  cord;  so  a  strong  activity  in  the  cerebral  cortex  tends  to  inhibit  the 
activity  of  the  rest  of  the  cortex  and  to  dominate  consciousness.  This  strong  local  cortical 
activity  is  accompanied  by  a  local  increased  blood  supply,  as  can  be  shown  by  the  ther- 
mopile. The  blood  supply  is,  therefore,  in  constant,  more  or  less  rapid  (usually  rapid)  ebb  and 
flow  throughout  the  different  areas  of  the  cortex,  being  most  abundant  in  those  areas  which  are  in 
activity. 

Consciousness  is  a  condition  which,  as  yet  certainly,  we  do  not  understand,  al- 
though in  a  general  way  we  regard  it  as  the  result  of  chemical  changes  taking  place  within  the  cere- 
bral cortex.  The  chemical  changes  themselves  are  not  consciousness,  but  they  produce  this  form 
of  nervous  energy  very  much  as  a  steam  boiler  and  a  dynamo,  or  a  galvanic  battery,  produces  elec- 
tricity. We  are  as  ignorant  of  the  exact  nature  of  consciousness  as  we  are  of  that  of  electricity. 
These  chemical  changes  produce  consciousness  (or  rather  the  perceptions  and  emotions 
which  constitute  it),  a  form  of  nervous  energy;  just  as  the  chemical  changes  taking  place  in  any 
living  cell  or  tissue  of  the  body  produce  a  form  of  energy  peculiar  to  itself.  Consciousness  is  thus 
locally  and  continually  produced  in  the  brain.  The  cortical  activity  causing  it  passes  according  to 
definite  channels  to  other  regions  of  the  cortex,  surges  through  the  brain,  awakening  memories 
and  ideas  and  causing  actions  and  reactions.  The  subject  is  a  most  difficult  one  and  is  made,  in  a 
sense,  more  difficult  by  the  ambigviities  of  language,  which  allow  us  to  replace  an  idea  by  a  word  of 
somewhat  uncertain  definition  and  thus  leads  to  uncertain  and  faulty  reasoning,  or  to  a  high 
sounding  sentence  which  means  nothing.  Consciousness,  or  cognition,  seems  to  be  something 
added  on  to  the  essential  processes  taking  place  in  the  brain.  The  various  association  reflexes 
occurring  in  the  brain  could  take  place  and  do  take  place  quite  accurately  without  consciousness, 
as  for  instance  in  the  automatic  acts  of  the  somnambulist,  or  in  the  epileptic  trance. 

That  consciousness  has  any  power  to  influence  cerebral  activity  and  the  association  reflexes  is 
not  evident  and  has  not  been  proved.  That  frequently  it  cannot  do  so  is  proved  by  the  oft  recur- 
ring condition  where  an  idea  is  present  in  consciousness  which  the  person  is  anxious  to  dismiss 
but  his  consciousness  even  combined  with  his  so-called  will  power  is  unable  to  dismiss  it.  Only 
when  by  the  association  fibers  a  different  and  stronger  local  cortical  activity  is  awakened  will  the 
distressing  idea  fade  away. 

The  brain  is  very  abundantly  supplied  with  blood,  e.specially  the  cortex,  and  the  latter  is  very 
sensitive  to  any  interference  with  its  blood  supply.  Loss  of  consciousness,  which  occurs  nor- 
mally in  sleep  and  pathologically  in  many  conditions,  is  caused  much  more  frequently  by  a  change 
in  the  quantity  (anemia)  or  quality  (drugs  and  poisons,  including  sepsis  and  other  autogenetic  toxic 
products)  of  the  blood  supply  than  by  all  other  conditions  combined.  Perver.sions  of  conscious- 
ness, on  the  other  hand,  seem  to  depend  less  upon  the  quantity  of  the  blood  .supply  than  upon  its 
quality  (poisons)  and  upon  changes,  organic  or  functional,  in  the  cerebral  cortex,  especially  upon 
its  exhaustion. 

Finally  it  is  to  be  remembered  that  the  cortical  cellular  activities  not  only  accompany  (are  the 
cause  of)  but  precede  sensation,  consciousness  and    the    other    "osychic"    functions.      The     con- 

20 


ditioned  reflexes  are  cortical  activities,  but  they  occur    in    infants    and    animals  unconsciously  and 
prior  to  any  e^ndence  that  the  "psychic"  functions  as  yet  exist. 

Emotions   (Chart  III  and  IV) 

The  great  majority  of  sensations  perceived  by  an  individual  during  his  life  are  followed  by 
the  reactions  in  the  nervous  system  already  described.  There  are,  however,  sensations  and  per- 
ceptions which  are  accompanied  by  an  emotional  content — pleasure  or  pain,  according  as  their  con- 
tent suggests  the  well-being  of  the  body,  a  richer  and  happier  life  on  one  hand;  or  death,  or  a  re- 
stricted and  unhappy  life  on  the  other  hand.  Heredity,  early  education,  past  experiences  and  asso- 
ciations, also,  influence  the  emotional  content  of  a  perception.  Such  perceptions  with  an  emotional 
content,  cause  an  abnormally  powerful  reaction  on  the  part  of  the  nervous  system.  The 
emotional  reflexes  are  among  the  earliest  to  be  observed  in  the  infant.  It  appears  from  experi- 
ments on  animals  that  the  emotions  of  pleasure  are  the  result  of,  or  at  least  are  influenced  by,  cortical 
activity;  while  the  emotions  of  pain,  anger  and  displeasure  occur  after  the  removal  of  the  cerebral 
hemispheres  and  are  the  result  of  the  activity  of  the  basal  ganglia.  These  emotions  produce  a  strik- 
ing effect  upon  the  functions  of  the  abdominal  viscera  as  has  been  abundantly  proved  by  animal 
experimentation  and  human  experience.  Thus,  pleasant  sensations  promote  the  activity  of  the 
muscles  and  glands  of  the  stomach:  while  unpleasant  sensations  retard,  or  entirely 
arrest,  this  activity.  But,  by  far,  the  most  striking  and  important  influence 
of  the  emotions  upon  the  somatic  activities  is  that  manifested  by  anger  and  fear  upon 
the  secretion  of  the  suprarenal  glands  and  the  consequent  rapid  and  excessive  production  of 
adrenalin.  The  emotions  of  anger  and  fear  are  usually  followed  by  violent  muscular  activity 
whether  in  the  form  of  fighting  or  flight.  It  has  been  proved  by  experimental  and  clinical  evi- 
dence that  adrenalin  appears  in  increased  quantity  in  the  blood  within  a  few  seconds  or  a  few 
minutes  after  the  occurrence  of  violent  anger  and  fear.  Furthermore,  it  has  been  proved  by  ex- 
periment that  adrenalin  in  excess  in  the  blood  causes  first  an  increase  in  the  amount  of  sugar  in  the 
blood  which  is  essential  for  muscular  contractions;  second,  a  dilatation  of  the  bronchioles  and  in- 
creased rapidity  and  power  of  the  heart  action,  thus  causing  an  increased  amount  of  oxygen  in  the 
blood  which  is  also  essential  for  muscular  contraction ;  third,  prevents  muscular  fatigue  and  re- 
stores power  to  exhausted  muscles,  and  fourth,  quickens  coagulation  of  the  blood.  All  of  these 
conditions  are  of  great  practical  value  to  the  angry  or  frightened  animal,  whether  in  a  fight  or  in 
a  flight. 

In  addition  to  these  violent  emotions,  there  are  more  gentle  emotions  of  pleasure  and  pain 
which  we  call  "feelings"  and  which  are  due  in  part  to  internal,  or  general,  sensations  from  the  body 
itself  and  in  part  from  the  success  or  failure  of  our  undertakings  in  life.  When  the  bodily 
functions  are  disordered  we  have  a  general  feeling  of  discomfort  and  when  all  is  working  well  we 
have  a  sense  of  buoyancy  and  exaltation;  all  moves  smoothly  without  friction,  as  in  a  well  oiled 
machine.  These  internal  sensations,  as  was  mentioned  on  a  previous  page,  are  ordinarily  the 
dominant  factor  in  our  feelings  and  emotions  and  greatly  influence  also  our  voluntary  actions, 
which  for  instance  may  be  altogether  different  in  a  state  of  hunger  from  those 
in  a  state  of  satiety.  Indeed  the  internal  sensations,  such  as  hunger,  etc.,  are 
very  often  themselves  the  cause  of  extensive  voluntary  acts,  which  usually  result 
in  the  relief  from  this  sensation.  As  these  internal  sensations  vary  from  time  to  time,  our  moods 
change,  and  perceptions,  which  at  one  time  are  pleasant,  may  at  another  time  be  unpleasant.  Ir- 
respective of  our  moods,  however,  some  perceptions  are  almost  always  pleasant,  others  are  not. 
Things  which  tend  towards  the  preservation  and  health  of  oneself  and  one's  family  are  usually 
pleasant  and  vice  versa.  Perceptions  to  which  we  have  become  accustomed  are  usually  pleasant, 
and  even  unpleasant  perceptions  by  frequent  repetition  at  times  become  bearable  and  even 
pleasant. 

Not  a  few  perceptions  are  accompanied  with  relief  or  discomfort,  as  when  hunger  is  as- 
suaged, or  we  accomplish  something  desired,  or  in  some  way  contribute  to  our  well-being  or  suc- 
cess and  thus  give  pleasure;  while  other  perceptions  act  in  a  contrary  manner.  These  feelings  of 
pleasure  and  pain  may  be  due  in  part  to  the  intensity   of   the   sensation   or   perception ;  in  part  to 

21 


heredity,  as  a  result  of  evolution,  in  the  case  of  objects  desirable  for  the  health  of  the  body;  but  in 
greater  part  to  associations  (see  Association)  with  previous  similar  perceptions,  and  in  greatest 
part  to  feelings  of  satisfaction  or  dissatisfaction  with  the  result  of  one's  actions. 

Sensations  of  moderate  intensity  are  usually  pleasant;  sensations  of  very  great  intensity 
which  produce  abnormally  strong  reactions  in  the  nervous  tissues,  are  usually  unpleasant,  while 
those  wliich  liave  a  complicated  ratio  are  usually  also  unpleasant,  which  is  especially  true  for 
musical  sounds.     Foods  which  nourished  our  ancestors  usually  taste  good  to  us. 

The  child  possibly  acquires  a  taste  for  sweet  things  from  the  sugar  in  its  mother's  milk.  Most 
of  our  pleasant  and  unpleasant  sensations  are  the  result  of  our  education.  They  are,  therefore, 
much  more  pronounced  in  adults,  especially  educated  ones,  than  they  are  in  children ;  although  the 
expression  or  manifestation  of  them  is  less  pronounced,  more  inhibited  or  restrained  by  other 
cortical  activities.  A  perception  which  is  associated  with,  or  followed  by,  pleasure  or  pain  will 
always,  or  for  a  long  time,  as  often  as  it  occurs  actually  or  in  memory,  be  accompanied  by 
a  pleasant  or  painful  emotion,  whether  the  memory  of  the  original  pleasant  or  painful  result 
associated  with  it  is  present  in  consciousness  or  not. 

On  the  other  hand,  our  emotions  or  rather  "our  moods,"  depend  in  great  part  on  our  success 
or  failure  in  life.  Mankind  does  not  find  itself  in  this  world  with  all  its  needs  and  wants  satis- 
fied; on  the  contrary,  everyone  must  acquire  food,  clothes,  habitation,  warmth  and  a  hundred  other 
necessities.  A  man  who  sees  his  neighbor  with  something  good,  which  he  has  not,  desires  it,  or 
something  similar.  These  wants  and  desires  are  the  great,  almost  the  only,  incentives  to  volun- 
tary action.  When  tliis  voluntary  action  results  in  success  we  have  in  it  our  greatest  pleasure 
and  when  it  results  in  failure,  our  greatest  unhappiness.  All  things  connected  with  our  success 
receive  an  associated  emotion  of  happiness;  while  those  things  connected  with  our  failure  receive 
an  associated  emotion  of  grief. 

In  these  various  ways  a  certain  number  of  our  perceptions  have  associated  with  them  an 
emotion  (204),  or  mood,  or  tone,  of  pleasure  or  pain,  greater  or  less,  and  a  series  of  such 
emotions,  or  one  long  continued,  will  make  us  happy  or  unhappy  for  a  considerable  length  of  time 
and  will  constitute  what  we  call  our  "mood." 

In  certain  abnormal  states  of  the  cerebral  cortex  (exhaustion,  circulatory  irregularities, 
poison  and  other  less  known  disorders)  the  emotions  become  dissociated  from  the  ideas  with 
which  they  are  normally  associated ;  so  that  all  cerebral  activity'  is  accompanied  by  one  emotion : 
in  some  cases,  sadness;  in  others,  fear;  in  others,  joy  and  in  others  apathy  or  absence  of  all 
emotion.  An  emotion  is  often  so  strong  and  so  occupies  the  patient's  consciousness  that  it  is  im- 
possible, or  nearly  so,  to  attract  his  attention.  Such  an  abnormal  mental  condition  occurs  in  some 
forms  of  insanity. 

Association 

The  essential  physiological  characteristics  of  nervous  tissue  are:  first,  its  excitability,  its 
reaction  to  .stimulation  by  the  discharge  of  nervous  energy  stored  within  it,  and  second,  its 
transmissibility ;  this  nervous  energy,  wherever  produced,  does  not  remain  localized,  but  tends 
to  pass  along  nerve  fibers,  throughout  its  own  neurons  and  to  other  neurons.  The  channels  along 
which  it  will  pass  depend  upon  the  anatomical  arrangement  of  the  fibers.  In  consequence 
of  heredity  and  evolution,  certain  channels  are  easier  for  the  passing  of  this  nervous  impulse 
than  are  others.  This  is  especially  true  of  certain  reflexes  present  at  birth,  such  as  breathing,  suck- 
ing, etc.  Other  channels  are  made  easy  later  in  life  by  the  constant  passage  of  impulses  along 
them.  The  more  frequently  an  association  fiber  and  the  synapse  connecting  two  fibers  are  used  the 
better  conductors  they  become.  The  way  that  has  once  been  traversed  and  that  has  often  been 
traversed  becomes  the  easiest  way.  It  is  the  way  of  least  resistance  and  it  is  a  universal  rule, 
whether  it  be  a  foot-path  or  a  conductor  of  electrical  or  of  other  force  or  a  nerve  fiber  or  cell 
or  a  synapse  separating  two  cells,  that  the  way  of  least  resistance  is  the  easiest  way:  the  way 
usually  followed.  When  not  used  for  a  long  time,  like  a  deserted  garden  path,  the  cliannel  may 
be  obliterated  and  the  association  lost. 

When  a  perception  occurs,  impulses  radiate  out  along  the  association  fibers  from  that  por- 
tion of  the  cortex  which  produces  it.     If  at  the  same  time  another  perception,    (usually  there  are 

22 


many),  or  a  vivid  memory  of  a  perception  received  a  moment  before,  takes  place  in  another  por- 
tion of  the  cortex,  the  association  fibers  connecting  these  two  or  more  portions  of  the  cortex,  where 
perceptions  are  occurring,  or  have  just  occurred,  being  acted  upon  at  both  ends,  will  convey  im- 
pulses to  and  fro  more  readily  than  the  other  association  fibers.  The  details  of  this  process  are  ob- 
scure, but  it  seems  evident  tliat  the  longer  and  more  frequently  the  association  fibers  are  traversed 
by  these  impulses  the  better  conductors  do  they  become  and  these  two  perceptions  become  more  and 
more  easily  excited  the  one  from  the  other.  They  may  also  be  excited  through  the  mediation  of  a 
third  memory  associated  with  both  of  the  others.  The  activity  in  the  cortex  does  not  long  persist; 
so  that  when  the  associated  idea  is  in  consciousness,  the  original  perception  which  awoke  it  is  al- 
ready, or  soon  will  be,  subconscious.  Yet  they  are  firmly  associated  together;  so  that  whenever 
in  the  future  one  enters  into  activity  it  may  excite  the  other.  Thus,  association  between  percep- 
tions of  the  events  and  objects  received  simultaneously,  or  immediately  before  or  after  each  other, 
are  formed  in  a  never-ending  stream  and  the  events  and  objects  are  considered  as  contemporane- 
ous and  often  as  related  to  each  other.  Subsequent  experiences  may  verify  and  strengthen  some 
of  these  associations  and  may  disprove  and  unmake  others.  Associations  with  any  one  perception 
may  be,  and  usually  are,  extremely  numerous.  There  is  also  an  association  of  words  as  well  as 
of  perceptions  and  the  associations  of  words  have  no  necessary  relationship  to  the  associations  of 
the  objects  which  they  represent.  Associations  may  be  at  first  very  imperfect  and  very  difficult 
to  form,  but  with  repetition  and  practice  become  easy.  The  work  of  a  child  in  school  is  difficult 
until  by  repetition  he  has  learned  thoroughly  his  lesson.  Then  the  recitation  is  easy.  Addition 
subtraction,  etc.,  are  at  first  performed  slowly  and  with  difficulty  but  later,  in  consequence  of  fre- 
quent repetition,  rapidly  and  easily.  The  association  between  question  and  answer  becomes 
firmly  established. 

When  a  number  of  perceptions  are  produced  which  are  very  similar  and  yet  show  more  or 
less  individual  variations,  as  for  instance  perceptions  of  men  or  dogs,  from  a  comparison  of  them 
and  of  memories  of  others,  more  or  less  similar,  a  concept  or  idea  of  a  man  or  a  dog  is  formed 
which  includes  all  the  individuals.  From  many  examples  of  individual  freedom  of  action,  the 
abstract  idea,  or  abstraction,  of  liberty  is  formed.  A  great  many  such  abstract  ideas  are  gradu- 
ally formed  and  this  process  is  facilitated  by  the  use  of  language.  But  each  idea  is  the  result 
of  experience:  the  result  of  a  conglomeration  or  generalization  of  one  or  more  perceptions  and 
their  associations,  and,  by  the  aid  of  language,  is  given  a  name.  It  has  been  said  that  "we  caa 
understand  only  so  much  of  an  abstraction  as  we  know  individual  cases  which  sustain  it."  Think- 
ing and  reasoning  are  much  simplified  and  made  more  rapid  by  the  employment  of  these  abstrac- 
tions. A  concept,  idea,  or  abstraction,  differs  in  different  persons  in  consequence  of  their  different 
experiences,  of  their  education  and  of  their  associations  with  the  perceptions  involved. 

Ethics 

Inasmuch  as  the  sensory  and  motor  areas  of  the  cortex  are  intimately  connected  together, 
some  perceptions  lead  to  voluntary  action,  which  may  result  in  pain,  either  directly  as  physical 
pain,  or  indirectly  as  mental  pain,  the  result  of  punishment  or  condemnation ;  so  that  the  action 
and  the  perception  which  led  to  it  will  become  associated  with  these  unpleasant  sensations  or 
perceptions,  and  these  associated  unpleasant  sensations  will  tend  to  restrain  further  similar 
actions.  Such  acts,  bringing  with  them  a  penalty,  will  be  called  wrong  and  there  will  gradually 
be  formed  a  large  number  of  associations  which  will  be  identified  with  the  ideas  of  punishment 
and  condemnation  and  which  tend  to  prevent  the  performance  of  wrongful  acts :  just  as  another 
combination  of  associations  which  have  become  associated  with  pleasure,  reward  or  praise, 
will  be  associated  with  good  or  right.  A  person's  idea  of  what  is  right  or  wrong  will  depend 
upon  his  education,  the  result  of  experience  and  of  teaching,  and  is  the  basis  of  emotions  and 
ethics,  and  that  ill-defined  acquisition  from  teaching  and  experience,  the  so-called  conscience, 
and  may  evolve  into  very  elaborate  and  very  controlling  feelings  and  habits  of  thought.  Accord- 
ing as  education  has  developed  in  a  person  one  set  of  these  associations  rather  than  the  other,  a 
good  or  bad  character,  not  from  the  person's  own  but  from  the  community's  standpoint,  is  formed. 

23 


These  ethical  ideas  can  of  course  be  imparted  from  one  person  to  another  by  language  and,  indeed, 
frequently  are  so  imparted,  but  such  etliical  ideas  are  rarely  so  firm  and  convincing  as  those  ob- 
tained from  experience. 

Concentration  and  Attention 

It  seems  to  be  a  general  law  in  the  physiology  of  the  nervous  system  that  when  there  is  a 
stron"  activity  in  one  part,  the  activity  of  the  rest  of  the  nervous  system  is  inhibited.  Thus,  reflex 
activity  can  be  inhibited  by  strong  pain ;  and  the  reflex  activity  of  the  spinal  cord  is  more  or  less  in- 
hibited when  the  brain  is  in  activity.  In  the  brain  itself,  when  a  portion  of  the  cortex  or  a  group  of 
ner\-e  cells  is  in  activity,  the  activity  of  the  other  cortical  areas,  as  well  as  that  of  the  lower  centers, 
is  inliibited.  The  stronger  the  local  activity,  the  greater  and  more  extensive  will  be  the  general  in- 
hibition, and  consequently  the  more  this  local  activity  will  have  a  free  and  uninterrupted  field. 
When  an  unusual  or  very  vivid  perception  or  idea  is  in  consciousness  it  occupies  the  center  of  the 
stao-e.  Consciousness  consists  of  this  one  vivid  idea  and  its  associations;  so  that  milder  activities 
occurring  in  the  cortex  at  the  same  time,  which  should  produce,  ordinarily,  perceptions  and  asso- 
ciations, remain  subconscious.  This  phenomenon  is  called  concentration  and  is  a  very  important 
function  in  nervous  physiology.  When  the  cause  of  this  concentration  is  a  perception,  in  ad- 
dition to  this  inhibitory  influence,  impulses  from  the  active  sensory  cortex  radiate  to  the  motor  cor- 
tex and  out  to  the  perceiving  organ  and  cause  a  change  in  its  musculature  in  the  form  of  greater 
tension,  tonicity,  change  in  its  position,  etc.,  which  local  changes  heighten  the  power  of  the  organ 
for  the  perception  of  stimuli.  Concentration  is  only  another  name  for  attention  and  has  been  re- 
garded as  an  efi^ort,  and  an  expression,  of  the  will  or  will-power,  but  the  primary  and  essential  factor 
seems  to  be  unusually  strong  cortical  activity.  Not  infrequently  the  concentration  is  centered 
about  an  unpleasant  idea,  from  the  thought  of  which  we  vainly  try  to  escape;  yet  it  is  forced  upon 
our  attention  and  we  cannot  free  ourselves  from  it  in  spite  of  every  effort  of  our  so-called  will. 
We  are  at  times  in  a  state  of  "expectant  attention"  in  regard  to  some  possible  unpleasant  percep- 
tion, which  state  we  cannot  prevent,  try  as  we  may. 

Reverie  and  Thought 

The  steady  stream  of  perceptions  originating  from  the  excitation  of  the  various  sensory  or- 
gans is  constantly  awakening  associated  memories,  and  tliese  memories  other  associated  memories, 
and  so,  while  consciousness  remains  passive,  (does  not  for  the  moment  contain  any  strong  or  im- 
pelling idea)  an  ever-varying  series  of  memories,  visions,  day  dreams,  etc.,  flow  by.  This  is 
called  a  reverie  or  a  day  dream.  But  during  this  passive  condition,  some  memory  may  be  awak- 
ened which  will  arouse  a  number  of  associated  memories  (strong  cortical  activities)  which  will 
dominate  consciousness  and  may  pass  to  the  motor  area,  producing  action.  Tliis  stronger  cortical 
activity  brings  the  faint  or  passive  consciousness  into  a  strong  active  condition  of  attention  and 
the  passive  reverie  will  be  converted  into  active  thought  and  this  latter  condition  is  called  the  act 
of  fhmklng  or  reasoning.  The  process  of  thinking  is,  thus,  independent  of  speech;  although  speech 
is  essential  to  its  clear  expression  and  certainly  facilitates  it,  especially  in  its  deep  and  profound 
forms.  The  question  of  attention  is  one  which  seems  to  require  a  more  or  less  external  will  to 
keep  the  cerebral  activity  limited  to  one  subject.  Attention  is,  however,  a  manifestation  of  the 
activity  of  the  association  of  ideas.  If  many  associations  at  the  same  time  bring  into  strong  con- 
sciousness the  desirability  of  investigating  some  one  perception,  this  idea  (desirability  of  investiga- 
tion), which  we  may  call  "a"  and  which  will  have  widespread  associations,  will  bring  into  con- 
sciousness this  perception  to  be  investigated,  which  wc  may  call  "b"  with  its  various  associations. 
If  one  of  these  associations  leads  to  others  remote  and  unrelated,  and  away  from  "b"  it  will  not 
go  far  before  it  will  awaken  some  of  the  associations  conected  with  "a,"  even  the  absence  of 
"b"  from  consciousness  will  do  tliis,  and  "a"  will  be  brought  into  consciousness  and  through  "a" 
the  investigation  will  be  brought  back  to  "b"  again.  This  action,  like  other  nervous 
actions,  grows  stronger  by  use,  just  as  a  machine  runs  more  .smoothly  and  powerfully 
after  its  initial  stiffness  has  been  overcome  by  use;  so  a  trained,  educated,  cerebral  cortex,  is  able 

24 


to  keep  one  set  of  memories  present  in  consciousness  (attention),  to  call  up  associated  memories, 
to  reject  some,  to  keep  others  active  and  to  compare  them  all  together. 

When  we  have  forgotten  a  name,  we  often  cannot  by  an  effort  of  "will,"  however  strong,  re- 
call it.  The  desire  for  the  name  starts  series  after  series  of  associations  in  some  way  related  to 
the  name,  which  finally  bring  it  into  consciousness.  Or  the  attempt  may  fail  and  the  desire  may  be 
unsatisfied  at  the  time.  Hours  or  days  afterwards  the  name  may  enter  consciousness  by  some 
chance  conscious  or  subconscious  association  and  be  recognized  as  the  desired  name. 

Imagination  :  Creative  Faculty 

A  perception  usually  calls  up  memories  previously  associated  with  itself  or  its  memory.  But 
unrelated  memories  may  have  previously  been  in  consciousness  simultaneously,  or  nearly  so,  and 
these  memories  may  associate  themselves  with  it  and  a  combination  of  ideas  and  scenes  may  pre- 
sent themselves  which  are  not  the  result  of  any  unmodified  previous  experience.  This  is  called 
imagination.  Imagination  is  based  upon  memory.  We  can  imagine  nothing,  the  elements  of  which 
we  have  not  previously  perceived.  But  memory  can  present  elements  not  previously  associated 
together  (men  and  wings)  and  these  elements  may  combine  themselves  to  produce  a  non-existing 
entity :  i.  e.,  men  with  wings.  Things  may  be  so  combined  and  modified  as  to  produce  an  entity, 
strange,  bizarre  and  never  before  perceived.  The  normal  relations  of  parts  may  be  altered  out  of 
all  relationship  to  themselvs  to  produce  something  quite  different  from  anything  within  our  ex- 
perience. Thus,  things  may  be  combined,  which  are  the  exact  opposite  of  our  experience, 
with  very  whimsical  results.  A  new  and  not  previously  perceived  possible  grouping  of 
well  known  elements  may  lead  to  experiments  and  discoveries  of  important  facts,  ideas,  theories, 
etc.  This  is  the  creative  "faculty"  which  shows  itself  actively  in  prose  and  poetic  works  of  the 
imagination,  in  contradistinction  to  true  facts  or  real  liistory,  and  passively  in  day  dreams.  This  re- 
sult of  cortical  activity  may  in  many  persons  be  facilitated  by  the  action  of  drugs  and 
may  in  some  cases  be  the  cause  of  hallucinations  and  delusions,  (as  in  hysteria,  hypochondriasis  and 
insanity).  However  strange  the  results  of  the  imagination,  the  elements  of  these  results  (even 
of  some  of  the  most  monstrous  delusions)  are  former  experiences. 

Intelligence  (Charts  III)' 

Intelligence  consists  of  the  contents  of  object  consciousness.  It  implies  accurate  formation  of 
associations  and  their  ready  future  availability.  It  is  absolutely  dependent  upon  memory,  without 
which  it  cannot  exist.  The  greater  the  number  of  memories  and  the  more  perfect  and  easier  the 
recalling  of  associations,  the  greater  is  the  intelligence.  A  person's  memories  depend  primarily  on 
perceptions  derived  from  his  sensory  organs  and  on  his  experiences.  The  greater  the  number 
and  the  variety  of  his  experiences  the  greater  will  be  his  intelligence,  other  things  being  equal.  If 
any  one  sensory  organ  is  absent  or  diseased  from  birth,  memories  of  this  sense  will  not  be  present 
and  the  intelligence  will  be  diminished,  unless  this  defect  is  in  some  way  compensated  for.  In- 
telligence does  not  necessarily  imply  keenness  of  perception. 

An  increase  of  intelligence,  though  unusual,  is  not  abnormal.  In  some  cases  this  increase  is 
due  to  a  greater  number  of  perceptions  and  ideas  (the  learned  man)  ;  in  some  cases  to  better  and 
vrider  associations  throughout  the  entire  sensory  cortex  (the  wise  man),  and  in  some  cases  one 
portion  of  the  cortex  is  functionally  developed  at  the  expense  of  others  (the  genius.) 

A  diminution  of  intelligence  may  be  due  to  imperfect  development,  to  impaired  nutrition  or 
to  destructive  lesions  of  the  cortex.  Perversions  of  intelligence  (insanity),  although  they  may, 
in  part,  be  caused  by  peripheral  lesions,  are  fundamentally  due  to  disease  or  poisoning,  or  malnu- 
trition of  the  cerebral  cortex. 

Personality   (Charts  III  and  XVI) 

Personality  is  a  term  used  to  express  all  the  energy  and  power  which  have  been  stored  in  the 
cerebral  hemispheres  by  the  activity  of  the  cerebral  cortex  during  the  life-time  of  the  individual.  It 
consists  of  all  his  memories,  sensations,  perceptions,  concepts,  ideas,  and  their  various  associations, 

25 


which  vary  in  character  in  different  individuals.  More  especially,  it  consists  of  those  strong  as- 
sociations which  have  become  his  habits  and  his  habitual  judgments  and  also  of  his  emotions,  and 
of  all  else  that  the  cerebral  cortex  and  its  association  fibers  have  accumulated  within  themselves 
in  virtue  of  their  activity  resulting  from  the  sensory  excitations  which  it  has  received  during  the 
individual's  experiences  in  his  life.  The  possibility  of  this  accumulation  by  the  cortex  and,  to 
some  extent,  its  character  depend  upon  the  hereditary  structure  and  functional  activity  of  the 
nervous  system  of  the  individual. 

Personality  is  the  sum  of  the  conscious  and  subconscious  content  of  the  brain.  It  expends 
as  this  content  grows  larger  and  better  systematized.  It  becomes  greater  as  during  life  a  larger 
stock  of  energy  is  accumulated  in  its  associated  memories.  It  is  stronger  as  the  consciousness  is 
more  intense  (\irility).  The  "Ego"  is  the  result  of  a  long  series  of  experiences  (former  per- 
ceptions) by  which  the  body  is  differentiated  from  the  external  world  (corporeal  ego),  and  by 
which  the  complex  of  memories  and  ideas  which  the  cortex  has  accumulated  is  differentiated  from 
that  of  other  individuals  and  is  peculiar  to  itself   (mental  ego). 

The  totality  of  one's  memories  constitutes  his  experiences.  Many  similar  memories,  or  ex- 
periences, are  gradually  combined  into  a  general  idea  or  principle  which  becomes  a  guide,  or  as- 
sociation channel,  for  future  judgments  and  actions  and  may  persist  after  the  individual  mem- 
ories or  experiences  upon  which  it  was  founded  have  been  lost.  Cortical  excitations  of  this  nature 
are  followed  at  once  by  actions  which  are  almost  involuntary  (habits)  and  are  not  the  result 
of  a  balancing  of  many  former  memories  and  ideas  (thought).  In  this  way  one's  character 
or  personality  is  built  up.  Ideas  firmly  fixed  by  tradition,  education  and  habit,  acquire  an 
overwhelming  emotional  value.  They  not  only  exist  in  spite  of  experience _biit_even  mould 
experience  into  conformity  with  themselves.  Personality  is  the  result  of  the  manifold  work- 
ing of  natural  forces.  Had  the  natural  forces  been  different  the  personality  would  have  been 
different.  Each  personality  has  its  own  history  founded  on  its  own  personal  experiences.  A 
man's  personality  is  not  present  at  birth.  It  has  been  acquired  or  created  during  and  by  liis  life 
reactions  in  a  brain  whose  organization  and  capacity  have  been  determined  by  heredity. 

Personality,  being  founded  on,  and  consisting  of,  personal  experiences,  is  strongly  individ- 
ual ;  but  inasmuch  as  the  large  majority  of  men  in  the  same  commimity  have  very  much  the 
same  experiences,  and  as  they  discuss  these  experiences  with  each  other,  there  springs  up  between 
them  a  friendly  feeling  as  beings  of  the  same  nature  and  with  the  same  interests,  needs,  desires 
and  aims.  According  to  its  education  from  its  experiences  a  personality  may  keep  itself  apart 
from  others  and  strive  only  for  its  own  well-being  and  may  thus  be  selfish  (an  egotist),  or  it 
may  merge  itself  into  the  social  life  of  the  community  and  strive  for  the  well-being  of  its  fellow 
men  as  well  as  its  own  and  thus  be  generous  (an  altruist).  In  spite  of  much  in  common,  each 
personality  differs  from  others.  Some  by  their  educational  experiences  become  contemplative 
men,  others  close  observers,  others  men  of  action,  etc.  Some  men  are  of  weak  character,  who 
have  always  been  indulged  and  have  always  followed  the  path  of  least  resistance;  some  are  of 
strong  character,  who  have  had  to  endure  privation  and  have  learned  to  control  their  desires. 
These  different  kinds  of  men  cannot  by  any  effort  of  will  change  suddenly  their  character,  which 
has  been  formed  slowly  by  countless  past  experiences,  acting  upon  a  brain  the  anatomical  struc- 
ture and  physiological  activity  of  which  has  been  determined  by  heredity.  The  personality  of  a 
child  has  the  jxitentiality  of  developing  in  the  future,  but  the  kind  of  development  depends 
as  much,  if  not  more,  upon  the  kind  of  future  that  is  before  it.  as  tipon  its  heredity. 

Personality  seems  to  be  the  energy  re.sulting  from  chemical  changes  which  have  taken  place 
and  are  taking  place  in  the  cerebral  cortex  and  to  depend  absolutely  upon  the  integrity  of  the 
latter.  When  the  cortex  is  exhausted,  or  diseased,  personality  may  be  changed  under  some  un- 
usual experience,  resulting  from  the  undue  dominance  of  some  local  excitation  of  the  cortex, 
either  permanently  or  temporarily  (double  personality),  or  it  may  become  completely  lost 
(automatism). 

There  is  no  scientific  or  trustworthy  evidence  of  the  existence  of  any  further  factor  in  the 
form  of  any  ethereal  essence,  a  "mind"  or  "soul,"    as    distinguished    from    what    has  been  de- 

26 


scribed  as  "personality."  Indeed  this  assumption  rather  complicates  than  simplifies  the  matter, 
inasmuch  as  it  is  contradictory  to  one  of  the  must  firmly  established  principles  of  natural  philos- 
ophy :  "the  law  of  the  censervation  of  energy."  This  law  has  not  only  been  established  by  ir- 
refutable proof  in  the  inorganic  world,  but  also  has  proved  by  experiment  to  be  valid  in  animals 
and  even  in  man.  If  the  soul  can  produce,  or  stop,  a  cerebral  activity  of  its  own  volition,  thus 
creating  or  annihilating  force  which  normally  proceeds  in  an  endless  chain  from  one  manifes- 
tation to  another,  then  the  law  of  the  conser\'ation  of  energj'  is  no  longer  valid. 

Mankind  has  been  unwilling  to  allow  that  the  casualties  and  laws  which  prevail  in 
physical  activities,  can  be  potent  also  in  the  body  and  still  less  in  the  brain  and  "mind,"  because 
this  controverts  all  their  preconceived  notions  of  the  soul  and  its  relation  to  God.  The  pre- 
judices (pre-judgments)  of  most  men  will  not  permit  them  to  regard  the  mental  activities  as  the 
result  of  the  physiological  activity  of  the  cerebral  cortex,  in  the  same  way  that  the  physiological 
activities  of  the  internal  organs  of  the  body  produce  and  cause  the  function  of  these  organs.  They 
are  unwilling  to  regard  psychology  as  identical  with  the  physiology  of  the  cerebral  cortex. 

In  earlier  historic  times,  the  winds  from  the  cardinal  points  of  the  compass,  rippling  streams, 
•cascades,  the  waves  of  the  sea,  growing  trees  and  shrubs,  etc.,  (everything  which  exhibited  mo- 
tion), were  each  supposed  to  be  animated  by  an  indwelling  spirit,  by  whom  their  motion  was 
originated  and  maintained.  At  the  present  time,  Naiads,  Nereids,  Dryads  and  other  Nymphs, 
charming  creatures  of  the  imagination,  have  all  been  banished  by  the  advance  of  knowledge. 
Only  the  indwelling,  animating  spirit  of  man,  the  soul,  still  survives  in  the  belief  of  many. 

If  a  needle,  or  bar  of  soft-iron,  is  rubbed  with  a  magnet,  or  with  a  piece  of  magnetic  iron 
ore,  and  suspended  so  that  it  can  turn  freely,  it  will  turn  towards  the  north.  A  philosopher  in 
very  ancient  times,  who  saw  this  phenomenon,  would  probably  have  said  that  this  iron  bar  con- 
tained an  animating  spirit  that  "willed"  to  turn  to  the  north  and  when  by  any  cause  it  was  de- 
flected it  still  willed  and  strove  to  turn  again  to  the  north.  A  modern  scientist  knows 
that  a  magnetized  iron  rod  tends  to  put  itself  at  right  angles  to  the  electric  currents,  which  are 
always  flowing  around  the  earth,  and  hence  it  points  north  to  the  magnetic  pole :  one  end  of  the 
axis  around  which  the  earth's  electric  currents  revolve.  He  has  proved  these  facts  by  many  ex- 
periments and  can  prove  them  again  at  any  time  ;  although  he  cannot  explain  the  final  cause  of 
the  action  of  the  earth's  electric  currents  upon  the  needle.  The  "why,"  he  does  not  know.  He 
does,  know,  however,  that  it  is  inevitable,  constant,  and  not  the  capricious  will  of  an  invisible  and 
unproved  spirit. 

Whether  an  individual  believes  in  a  soul,  or  not,  and  explains  the  phenomena  of  life  in  accord- 
ance with  this  lielief,  depends  upon  his  traditions,  his  education,  his  experiences  and  upon  the 
personality  which  has  been  gradually  created  and  developed  during  his  lifetime  by  the  com- 
bination of  all  those  forces  constituting  consciousness  and  subconsciousness,  and  which  per- 
sonality may,  in  a  sense,  be  likened  to  the  older  conception  of  the  soul.  It  seems  probable  that 
consciousness,  intelligence,  personality,  etc.,  are  forms  of  energy  and  may,  perhaps,  be  called 
spiritual  in  contradistinction  to  material.  They  certainly  are  absolutely  dependent  upon  the 
blood  supply  of  the  cortex,  and  when  this  is  arrested,  personality  with  every  other  manifestation 
of  consciousness  ceases;  but  it  still  exists  potentially  and  may  be  reanimated,  if  the  circulation 
be  restored  after  an  interval  of  only  a  few  minutes.  If,  however,  the  arrest  of  the  circulation  is 
so  long  that  the  cortex  begins  to  degenerate  or  die,  the  personality  is  lost  permanently,  both 
actively  and  fjotentially. 

Personality,  is  then,  the  energy  of  cortical  activity  accumulated  during  the  life  of  the  indi- 
vidual. It  is  the  sum  of  all  his  perceptions,  concepts,  their  associations  in  abstractions,  ideas, 
moods,  and  knowledge  and  the  demonstration  of  all  these  in  manner  and  method  of  action.  It 
is  the  so-called  mental  content  of  the  individual,  or  better  perhaps,  it  is  the  individual,  since  the 
functioning  of  all  his  organs  and  his  internal  secretions  are  factors  in  the  productions  of  his 
moods  and  are  peculiar  to  him.  It  is  the  "Ego."  As  it  is  energy,  not  matter,  it  may  be  re- 
garded as  the  mystic  spirit  called  the  "Soul,"  whose  manifestations  have  been  for  ages  the  rid- 
dle of  the  science  of  psychology  and  upon  whose  assumed  origin  and  destiny  has  been  built  the 
faith  of  religions. 

27 


Insanity   (Charts  III  and  XVI) 

There  is  an  abnormal  as  well  as  a  normal  cerebral  activity.  Whether  we  believe  in  the  ex- 
istence of  a  soul  within  the  body  or  not,  certainly  insanity  is  no  longer  regarded  as  the  posses- 
sion of  the  body  by  an  evil  spirit  (demoniacal  possession).  This  was  a  well  established  belief 
for  asjes,  but  it  has  long  since  been  abandoned  and  we  now  regard  insanity  as  caused  by  abnor- 
mal cerebral  action.  The  conception  of  the  control  by  a  spirit,  which  we  have  finally  rejected  as  re- 
gards insanity,  the  vast  majority  of  mankind  still  retains  for  the  healthy  body,  possibly  be- 
cause most  of  the  few  men,  who  really  think,  have  not  studied  cerebral  physiology. 

We  have  considered  briefly  the  actions  taking  place  in  the  sensory  area  of  the  normal, 
healthy,  cerebral  cortex.  In  an  abnormal  cortex  these  actions  are  deranged.  Local  disordered 
cortical  function  produces  local  paralysis,  or  apraxia,  or  convulsions,  or  even  hallucinations;  while 
general  disordered  function  produces  coma,  neurasthenia    or    insanity.  Abnormal      structure, 

whether  the  alteration  be  slight  or  great,  and  consequent  abnormal  function,  of  the  cerebral 
cortex  may  be  either  congenital  or  acquired.  The  congenital  form  may  be  manifest  in  early  in- 
fancy or  may  become  apparent  at  any  stage  of  the  individual's  development,  as  he  successively 
meets  tasks  which  require  more  and  more  intellectual  power,  when  it  becomes  evident  that  his 
intelligence  and  ethics  fall  below  the  commonly  accepted  standards  of  the  race  or  community  of 
which  he  is  a  member. 

Insanity  is  a  term  applied  to  those  forms  of  cerebral  activity  in  which  the  intelligence,  con- 
sciousness, emotions,  personality,  ethics,  etc.,  one  or  all,  are  absent  or  abnormal.  It  manifests 
itself  in  various  forms  of  cerebral  disorder  and  may  be  divided  into  two  classes:  the  organic  (or 
structuraf)  and  the  functional.  When  the  brain  is  congenitally  malformed  or  defective  in  con- 
sequence of  disease,  or  injury,  in  the  mother's  womb,  or  at  birth,  its  action  is  necessarily  impaired 
and  the  manifestations  of  its  activity  are  either  absent  or  abnormal.  Such  cases  are  evidently 
of  hereditary  or,  more  accurately,  of  congenital,  origin.  If  this  congenital  defect  be  extreme  and 
the  child  cannot  talk  he  is  called  an  idiot  (1083)  ;  if  the  defect  be  less  extreme  and  the  child  can 
talk  he  is  called  an  imbecile  (1090)  :  a  purely  arbitrary,  but  convenient,  division. 

Other  cases  of  congenitally  defective  brain  there  are,  which  are  capable  of  perceptions, 
memories,  associations  and  consciousness;  and  of  a  certain  degree  of  education. 
Some  are  even  precocious  children,  but  their  education  cannot  be  carried  very  far  and  at  about 
the  age  of  puberty  they  show  abnormal  cerebral  responses.  They  show  a  difficulty  in,  or  an  im- 
possibility of,  acquiring  the  more  complicated  concepts  of  morality,  altruism,  etc.  They  cannot 
form  wise  and  true  judgments  and  they  become  criminals,  moral  imbeciles,  etc.  These  cases  are 
classed  together  under  the  term  the  feeble-minded  (1094).  All  these  groups  of  congenitally 
defective  cliildren  constitute  the  class  of  amentia  (1078 — more  or  less  complete  absence  of 
a  mind  which  never  existed;  in  contradistinction  to  all  other  forms  of  insanity:  those  in  which 
intelligence  already  acquired,  more  or  less  perfectly,  is  lost,  more  or  less  completely,  and  which 
constitute  the  class  of  dementia  (1079). 

Education  and  training  have  much  to  do  with  the  development  of  the  activity  of  the  cerebral 
cortex  and  consequently  with  the  individual's  intelligence  and  ethics.  There  are  individuals  who, 
partly  in  consequence  of  a  defective  brain  and  partly  in  consequence  of  defective  training  and 
education,  do  not  have  normal  experiences  and  form  a  number  of  abnormal  associations  and 
ideas,  especially  etliical.  Such  individuals  comprise  the  majority  of  criminals  and  cranks. 
Such  cases  bridge  over  the  separation  between  the  congenital  and  the  acquired 
forms  of  insanity.  It  is  possible  that  a  person  with  a  normal  brain,  who  is  isolated  from  his  fel- 
low-beings and  receives  no  training  or  education,  will  be  feeble-minded  or  even  an  imbecile. 

In  amentia  the  cerebral  cortex  is  so  structurally  or  functionally  incapable  that  it  cannot  pro- 
duce perceptions,  or  register  memories,  or  form  associations,  except  of  the  most  rudimentary 
kind.  Persons  suffering  from  this  condition,  then,  have  no  material  for  intelligence,  conscious- 
ness or  ethics  and  are  either  incapable  of  any,  or  of  only  rudimentary,  speech.  In  dementia  an 
originally  fairly  normal  cortex,  in  consequence  of  organic    or    functional    disease,  can  no  longer 

28 


exhibit  sufficient  activity  to  bring  previously  acquired  memories  into  consciousness  or  to  repro- 
duce  formerly  acquired  associations  or  to  manifest  other   formerly   possible,  cerebral  activities. 

The  form  of  dementia  (loss  of  previously  acquired  intelligence)  most  closely  resembling 
amentia  is  adolescent  insanity,  or  dementia  precox  (1098),  wliich  occurs  in  apparently  normal 
youths  between  puberty  and  the  age  of  25  or  30  years.  They  lose  their  mental  and  physical 
activity,  and  exhibit  marked  mental  deterioration  and  consequent  abnormality.  Some  of  these 
cases  make  a  more  or  less  complete  improvement  and  are  able  to  lead  a  fairly  normal  life  of  rather 
subdued  intensity.     Other  cases  grow  worse  and  terminate  in  dementia  and  death. 

Still  other  cases  of  insanity  exhibit  a  fairly  normal  mentality  until  a  fairly  advanced  age,  at 
which  time  they  exhibit  delusions  and  erroneous  judgments,  from  wliich  they  construct  some- 
what elaborate  systetn-athed  delusions.  A  careful  consideration  of  the  history  of  such  cases 
shows  that  even  from  youth  they  have  exhibited  a  number  of  abnormal  judgments.  These  cases 
are  cases  of  paranoia  (1116)  and  are  incurable. 

In  addition  to  the  above  classes  of  cases,  in  which  the  dementia  is  usually  due  to  a  congenitally 
defective  brain,  is  a  class  of  cases  due  to  organic  disease  (lesions)  occurring  in  an  apparently  nor- 
mal brain  which  may,  however,  have  an  hereditary  tendency  to  cerebral  disease.  One  of  these 
forms  of  acquired  insanity  is  senUe  dementia  (1107),  which  is  due  to  atrophy  of  the  cerebral  con- 
volutions owing  to  imperfect  blood  supply,  which  is  itself  often  due  (secondarily)  to  atheroma- 
tous arteries  and  which  is  incurable.  Another  form  of  organic  brain  disease  eventually  cens- 
ing Atmentia.  is  general  paresis  (1106)  due  to  a  syphilitic  meningo-encephalitis.  Brain  tumors 
and  abscesses  and  meningitis,  may  also  in  rare  cases  give  rise  to  symptoms  of  insanity,  probably  by 
causing  local  or  general  disturbances  of  the  cerebral  circulation. 

These  cases  of  acquired  organic  brain  disease  terminate  in  dementia  and  death.  Dementia 
also  occurs  as  a  terminal  symptom  in  alcoholic  dementia  (1103),  epileptic  dementia  (1104), 
secondary  dementia  (1105),  and  in  most  other  forms  of  insanity  which  have  persisted  for  years. 
Exhaustion  of  the  cerebral  cortex  from  worry,  anxiety,  shock  and  other  causes  may  cause  in- 
sanity in  persons  with  an  unstable  brain,  as  may  also  an  anemic  and  altered  condition  of  the 
blood.  It  is,  of  course,  possible  that  several  of  the  above  causes  act  simultaneously,  or  in  se- 
quence, and  as  a  matter  of  fact  they  frequently  do  so. 

Many  forms  of  insanity  are  not  due  to  organic  brain  disease.  No  lesion  can  be  found  after 
death  and  they  must,  therefore,  be  classed  among  the  functional  diseases  of  the  brain.  Many  of 
these  are  due  to  poisons  (alcohol,  germ  toxins, ptomaines,  etc.),  others  are  due  to  mental  strain 
and  especially  to  all  possible  forms  of  worry,  in  persons  with  badly  educated  brains. 

In  most  of  these  functional  insanities,  acute  delirium  (1110),  delirium  grave  (1111),  con- 
fusional  insanity  (1108),  delirium  tremens  (1109),  Korsakow's  psychosis  (1102),  acute  alco- 
holic mania  (1112),  simple  delusional  insanity  (1113),  symptomatic  mania  (1114),  symptomatic 
melancholia  (1115),  the  cardinal  symptom  is  delirium,  frequently  associated  also  with  an  emo- 
tional disorder.  In  the  other  cases  of  this  group  there  is  a  profound  disorder  of  the  emotions 
alone  without  any  sufficient  rational  cause:  mania  (1118),  melancholia  (1117),  circular  insanity 
(1119),  manic-depressive  insanity  (1120.) 

We  have  already  considered  the  emotions  at  some  length.  The  emotions  may  at  times  attain 
such  an  intensity  as  to  entirely  dominate  the  personality  and  to  profoundly  influence  both  the 
thought  and  the  activity  of  the  patient  and  to  produce  clinical  pictures  of  mania  and  melancholia 
described  in  Chart  XVI. 

In  the  functional  insanities  characterized  by  delirium  we  meet  with  a  remarkable  class  of 
symptoms  called  illu.sions  (214)  and  hallucinations  (213),  which  are  present  usually  in  pro- 
fusion. Illusions  are  always,  and  hallucinations  are  frequently,  faulty  and  imperfect  percep- 
tions. Delusions  due  to  faulty  logic  or  faulty  premises  are  common  enough  in  the  congenital  and 
organic  insanities;  but  not  hallucinations  and  illusions,  although  they  do  occasionally  occur. 

An  hallucination  is  much  more  vivid  than  a  memory  and  is  not  a  complete  and  correct  re- 
production of  a  former  memory,  but  usually  is  something  strange  and  bizarre.  In  some  cases 
the  hallucinations  do  not  have  the  vividness  of  true  perceptions,  but  seem  to  be  internal  voices  or 

29 


suggestions,  telephonic  communications,  or  electrical  action,  etc.  The  process  in  the  brain  which 
produces  an  hallucination  must  be  similar  to  that  which  produces  a  perception  or  memory,  but 
the  process  is  limited  to  the  cerebral  cortex,  the  spino-peripheral  neurons  playing  no  part  in  it, 
as  they  do  in  a  perception.  Hallucinations  and  illusions  may  occur  as  the  result  of  a  local 
disturbance  in  a  brain  which  may  not  be  for  the  moment  entirely  normal,  although  the  individual 
is  certainly  not  insane.  In  such  cases,  hallucinations  and  illusions  can  be  quickly  dispelled  by 
reason  and  by  proof  of  their  abnormal  character.  Insane  persons,  however,  in  consequence  of 
a  diffuse  cortical  disturbance,  cling  to  their  hallucination?  and  illusions  with  great  tenacity  in  spite 
of  strong  proof  to  the  contrary.  They  cannot  be  corrected  by  the  evidence  of  their  other 
senses  or  by  the  evidence  and  reasoning  of  their  friends.  These  hallucinations  and  illusions  oc- 
curring in  a  brain  weakened  by  nature,  poison  or  disease,  naturally  lead  to  abnormal  associations 
and  consequently  to  abnormal  ideas  (delusions).  Abnormal  associations  will  result  not  only 
from  the  strength  and  vividness  of  these  hallucination.s,  but  also  because  from  patches  of  men- 
ingitis and  from  patches  of  atrophy,  or  other  cause,  in  the  brain  of  an  insane 
man  some  areas  of  the  cortex  have  more  blood  and  are  more  easily  excited  than 
others  and,  therefore,  respond  more  readily  to  association  impulses,  near  and  remote. 
Moreover,  these  abnormal  ideas,  entering  into  consciousness  and  coming  into  conflict 
with  former  long  established  ideas,  lead  to  a  condition  of  consciousness  which  we  call 
bewilderment,  clouded,  befogged,  confusion,  distrust,  apprehension,  fear,  etc.  In  these  cases 
impulses  reaching  the  cortex  normally  from  the  organs  of  sense  are  so  much  weaker  than 
the  excitations  already  there,  that  they  cannot  enter  into  consciousness,  but  remain  subconscious. 
They  may,  although  subconscious,  be  registered  and  may  be  recalled  to  consciousness  after  the 
attack  of  insanity  is  past,  but  they  have  no  present  value  and  are  inadequate  to  correct  the  abnor- 
mal activities  and  no  sane  judgment  can  result. 

A  cortex  in  which  normal  perceptions  can  occur  only  imperfectly,  or  not  at  all,  and  in  which 
abnormal  perceptions,  associations  and  ideas  are  dominant,  will  naturally  produce  abnormal  asso- 
ciation reflexes,  or  actions.  The  simplest  of  these  is  delirium  (217,  1109-10),  in  which  the 
patient  responds  by  word  and  act  to  the  many  false  perceptions  and  ideas  in  his  clouded  and 
weakened  con.sciousness.  When  the  intensity  of  the  process  is  less  the  false  perceptions  and 
ideas  will  produce  delusions  (215,  1097),  which  will  cause  abnormal  and  often  dangerous  asso- 
ciation reflexes  or  acts.  These  delusions  may  remain  isolated,  unsystematized  or  may  be  woven 
in  with  all  the  real  experiences  of  the  individual's  life;  so  that  a  systematized  delusion,  founded 
upon  more  or  less  evidence  or  reasoning,  acting  upon  a  weakened  or  limited  general  cortical  ac- 
tivity, and  one,  therefore,  incapable  of  producing  a  correct  judgment,  results. 

Often  in  justifying  or  explaining  a  delusion  a  patient  will  give  reasons  or  cite  experiences, 
which  we  call  false,  but  which  are  doubtless  experiences,  which  have  been  presented  to  him  by 
his  abnormally  acting  cerebral  cortex.  These  delusions,  or  false  and  imcorrectable  judgments, 
naturally  lead  to  acts  which  are  incompatible  with  an  unconstrained  life  in  a  reasonable  com- 
munity. Naturally,  with  all  these  abnormal  cortical  activities,  not  only  the  ethical  ideas  of  the 
individual  are  changed,  but  al.so  the  normal  emotions  associated  with  normal  cortical  activity  are 
profoundly  altered,  whether  in  the  form  of  exaltation  or  depression,  either  continuously  or  in 
alternation  with  each  other. 

In  all  forms  of  insanity,  in  consequence  of  its  abnormal  content,  consciousness  is  altered 
and  personality  may  be  changed.  There  may  be  a  double  personality  or  the  individual  may 
imagine  that  he  is  dead,  an  animal,  a  king,  or  God,  or,  in  extreme  degrees  of  dementia,  the 
patient  may  show  no  consciousness  or  personality  at  all.  The  emotions  are  also  altered  (morbid 
temperaments)  in  accordance  with  ideas  in  consciousness,  or  may  be  entirely  dissociated  from  the 
ideas  with  which  they  are  normally  in  harmony,  or  may  be  entirely  absent  in  extreme  dementia, 
or  may  be  feebly  carried  over  from  former  highly  emotional  states.  The  emotion  most  fre- 
quently present,  especially  in  the  early  stages  of  the  disease  is  fear  fphobia). 

Fear  and  apprehension  are  prominent,  even  dominant,  symptoms  in  the  early  stages  of 
almost  every  case  of  insanity.  The  unusual,  often  monstrous,  phenomena  occurring  in  the 
cerebral  cortex  are  so  different  from  those  previously    present   and    so  out  of  harmony  vrith  for- 

30 


mer  memories  and  ideas,  that  the  patients  naturally  become  distrustful,  apprehensive  and  full  of 
fear.  Many  can  hardly  believe  the  information  supplied  by  their  own  senses,  much  less  the  words 
of  their  friends^.  Some  regard  themselves  as  persecuted  and  as  the  victims  of  conspiracies. 
Fear  is  the  dominant  emotion  within  them. 

The  association  reflexes  are  always  altered  in  insanity  in  consequence  of  the  abnormal  cortical 
activity.  In  extreme  dementia,  voluntary  motion  is  completely  abolished.  In  profound  melan- 
cholia, voluntary  acts,  as  well  as  thought,  are  inhibited;  while  the  reverse  is  true  in  mania,  in  which 
cortical  activity,  although  abnormal,  is  greatly  exaggerated.  In  consequence  of  prominent, 
compulsory   ideas,   so   frequent  in   insanity,   compulsory  acts  result. 

Voluntary  Action.    Association  Reflexes 

The  ultimate  product  of  the  complex  mechanism  of  the  nervous  system  is  an  action  upon  the 
animal's  or  man's  environment  for  his  benefit.  We  have  already  considered  this  activity  in  its 
barest  outline  under  the  title  of  "cortical  reflexes."  It  seems  desirable  to  consider  these  re- 
flexes more  fully  in  the  light  of  our  knowledge  of  the  "psychic  activities"  and  under  the  name 
by  which  they  are  generally  known,  "voluntary  acts"  or  "association  reflexes." 

Activity  never  normally  originates  directly  or  spontaneously  in  the  motor  area  of  the  cerebral 
cortex,  but  the  cortical  impulse  initiating  the  movement  always  originates  from  the  sensory  area  of 
the  cortex.  When  a  very  strong  excitation  arises  in  this  sensory  cortex,  as  for  instance,  per- 
ceptions which  are  associated  with  the  idea  of  imminent  danger  of  death,  this  excitation  passes  to 
the  motor  cortex  and  thence  down  through  the  internal  capsule  and  pyramidal  tract  and  causes 
movements  of  flight  and  self-preservation.  This  act  is  as  inevitable  and  as  machine-like  as  is  the 
simplest  reflex  act.  A  good  swimmer  bent  on  suicide  cannot  drown  himself  unless  he  is 
weighted  or  the  action  of  his  arms  or  legs  is  restricted.  Escape  from  imminent  death  is  for 
most  men  an  imperative  voluntary  act.  If,  however,  the  danger  is  less  great,  as  on  a  battlefield, 
the  excitation  leading  to  flight  may  still  be  there,  but  it  may  be  inhibited  by  excitation  from  other 
associations,  such  as  the  idea  of  shame,  love  of  country,  etc.,  and  the  two  excitations  may  neutral- 
ize each  other.  It  is  a  question  in  any  individual  jcase  whether  the  chemico-physical  energies 
representing  and  causing  the  fear  of  death  or  those  representing  and  causing  love  of  country  and 
honor  are  based  on  stronger  experiences  and  wider  and  stronger  associations.  Whichever  is  the 
stronger  prevails. 

Ordinarily,  when  a  perception,  or  memory,  suggesting  action  has  sufficient  intensity  to  enter 
consciousness,  the  excitation  is  sufficiently  strong  to  pass  along  the  association  fibers  and  awaken 
into  activity  the  group  of  motor  cells,  called  the  "common  paths,"  lying  in  the  anterior  central 
convolution  and,  if  no  other  counteracting  excitation  comes  to  this  latter  portion  of  the  cortex, 
the  irritation  passes  through  these  great  motor  cells  in  the  anterior  central  convolution  and  down 
through  the  internal  capsule  and  pjTamidal  tract  and  the  action  takes  place.  Actions  resulting 
from  memories  are  usually  weaker  than  those  resulting  from  the  original  excitation  or  perception. 
When  a  number  of  more  or  less  conflicting  memories  and  ideas  are  in  consciousness,  some  for  and 
some  against  the  action,  impulses  will  be  constantly  coming  to  the  motor  cortex  to  be  either  im- 
mediately inhibited,  or  strengthened.  The  play  of  the  diiiferent  perceptions,  memories  and  ideas, 
the  play  of  motives,  nmy  continue  a  long  time  as  the  person  deliberates  and  exercises  his  free-mil. 
This  merely  means  that  the  sensory  activities  causing  the  diflferent  memories,  together  with  those 
causing  the  ideas  derived  from  the  mass  of  associated  memories  which  constitute  our  ethics  and 
those  which  constitute  our  emotions,  have  sufficient  intensity  to  act  upon  the  motor  cortex,  some 
as  excitants,  some  as  inhibitors.  Fresh,  allied  memories  constantly  enter  consciousness,  because 
of  their  association  with  those  already  in  it,  and  take  part  in  this  phenomenon.  It  is  like  a  de- 
bating society  in  which  arguments  for  and  against  are  presented  almost  simultaneously,  and  the 
stronger  argument  rather  than  the  will  of  the  judge  is  the  decisive  factor.  It  is  probable  also  that 
subconscious  activities  may  play  some  part  in  this  process  and  it  is  certain  that  the  emotions 
exercise  an  almost  dominant  part  in  it.  Eventually  the  stronger  excitation  will  prevail  and  the  act 
will  be  either  done  or  left  undone. 

31 


A  voluntary  act,  depending  upon,  and  being  the  result  of,  the  association  of  ideas,  may  be 
described  as  an  association  reflex.  The  idea  of  the  apparent  freedom  of  will  depends  upon  the 
absence  of  external  compulsion  and  also  upon  the  fact  that  the  action  takes  place,  or  does  not  take 
place,  in  accordance  with  the  relative  strength  of  those  cortical  activities,  which  cause,  also,  our 
ideas  and  desires.  The  more  perceptions  and  ideas  a  person  has  in  his  memory,  the  more  learned 
and  intelligent  he  is.  the  greater,  wider  and  more  protracted  will  be  this  "play  of  motives"  and 
the  more  difficult  will  be  the  choice  of  the  resulting  action :  the  victory  of  any  one  set  of 
motives.  The  very  learned  man  is  not  the  man  of  action.  In  a  child,  or  in  an  ignorant  man, 
with  fewer  elements  of  a  choice,  the  association  reflex  will  usually  be  more  prompt.  When  a 
decision  under  the  same  or  similar  conditions  is  made  a  second  time,  and,  especially,  when  fre- 
quently repeated,  the  association  reflex  takes  place  more  and  more  promptly.  In  the  frequent 
repetition  of  an  act,  practice,  the  same  conducting  channels  and  synapses  are  being  constantly 
traversed  and  consequently  become  better  conductors,  and  the  act  is  easier  to  perform  and 
is  more  or  less  automatic.  It  becomes  a  habit.  A  large  part  of  our  voluntary  acts  are 
habits.  It  is  to  be  remembered,  also,  that  the  internal  sensations  and  secretions  which  dominate 
our  "moods,"  exercise  a  strong  influence  over  voluntary  movements  which,  under  changing 
moods  and  altered  internal  sensations  and  secretions,  may  be  very  different  at  different  times, 
although  the  causal  external  sensation  is  the  same. 

The  gray  matter,  the  point  of  union  of  the  motor  and  sensory  neurons,  is  in  small  com- 
pass in  the  subcortical  centers  and  hence  is  well  fitted  for  direct  transference:  for  reflex  and  auto- 
matic actions.  In  the  cortical  centers,  the  gray  matter  is  spread  over  a  large  surface  and  per- 
mits separate,  local  action,  and  consequently  permits  a  large  number  of  different  memories  and 
ideas,  some  positive  and  some  negative,  to  act  simultaneously  upon  the  motor  cortex  and,  thus, 
either  cause  or  prevent  a  voluntary  action.  Both  voluntary  and  reflex  acts  are  for  the  benefit  of 
the  individual.  The  reflex  acts  depend  upon  heredity  and  evolution.  They  are  the  result  of  the 
experience  of  the  individual's  ancestors,  of  the  experience  of  the  race  (phylogenetic). 
Voluntary  acts  depend  upon  the  individual's  personal  experience  (ontogenetic).  The  difference 
between  the  two  depends  mainly  on  difference  in  anatomical  structure.  In  conditions  which  are 
new  and  in  which  no  experience  can  guide  him,  an  individual's  voluntary  acts  are  quite  as  likely 
to  be  detrimental  as  salutary.     His  reflex  acts  almost  without   exception  are   salutary. 

The  innervation  memories  stored  in  the  motor  cerebral  cortex  are  originally  acquired  from 
reflex  acts.  The  first  voluntary  acts  of  the  child  (sucking,  opening  and  closing  eyes,  closing  of 
hand,  etc.)  are  adopted  reflex  acts,  either  unmodified  or  but  slightly  modified.  A  young  infant 
does  not  will  to  suck  milk  from  his  mother's  breast.  It  is  a  reflex  act.  But  after  the  infant  has 
experienced  the  result  of  this  act  a  sufficient  number  of  times,  the  sight  of  his  mother,  or  hunger, 
may  awaken  his  memor-  ^f  this  act  and  of  the  consequent  relief  from  hunger,  may  awaken  his 
desire,  and  he  will  suck  the  breast  voluntarily  in  consequence  of  this  active  memory.  Voluntary 
motions,  or  association  r  -I  -.xes,  occur  early  and  develop  rapidly  in  infantile  life,  but  occur  much 
earlier,  though  they  develop  more  slowly,  in  young  animals.  Chickens  run  almost  as  soon  as  they 
are  born  to  their  mother  when  she  "clucks"  for  them.  The  lower  animals  thus  possess  at  birth, 
by  heredity,  a  more  perfect  nervous  sy.stem ;  while  human  infants  possess  at  birth  by  heredity, 
one  less  perfect,  but  capable  of  a  wonderful  development,  which  results  in  greater  part  from  per- 
sonal experiences. 

The  Play  op  Motives 

The  isolated  cortical  areas,  containing  the  memories  acquired  by  previous  experiences,  are  all 
brought  into  activity  by  association  fibers.  When  any  sensory  impulse  requiring  action  is  brought 
to  the  cerebral  cortex,  conflicting  ideas,  corresponding  to  those  localized  memories,  must  be 
brought  into  unison  before  any  association  reflex  (voluntary  action)  can  result.  The  cerebral 
activity  may  be  compared  to  a  town  meeting. 

At  the  town  meeting  a  new  condition  presents  itself  for  action.  Shall  some  action  be  taken,  or 
postponed,  or  refused?  The  subject  is  discussed  from  many  angles;  the  result  of  memories  stored 
in  the  sensorj^  area  of  the  cortex  of  the  citizens.  Many   ideas   acquired    from    former   experiences 

32 


are  advanced.  The  clergy  bring  forth  certain  moral  factors,  the  result  of  a  long  education  extend- 
ing back  to  infancy  when  the  brain  was  most  impressionable  and  which  have  long  been  pre- 
served in  the  brain  as  fixed  principles.  The  business  men  advance  certain  utilitarian  factors,  ex- 
periences acquired  through  many  business  undertakings  and  which  have  been  stored  in  the  brain 
as  fixed  business  principles  and  are  emotionless.  The  poets  and  orators  present  the  emotions  of 
patriotism  and  glory  which  have  been  the  result  of  a  long  education,  which  has  stressed  their  vital 
importance  for  the  community  and  each  individual  member  of  it.  The  shysters  and  rascals  pre- 
sent ideas  of  self-interest  and  pecuniary  expediency.  Each  view  advanced  calls  up  another,  favor- 
able or  unfavorable.  And  so  the  dispute  rages.  The  chairman,  or  moderator,  takes  no  part  in 
the  discussion,  wliile  all  these  different  ideas  are  poured  in  upon  him.  One  by  one  inadvisable 
or  impractical  ideas  die  away.  Their  tendency  to  action  is  inliibited  by  the  stronger  impulse  ot 
the  majority  of  other  ideas.  A  greater  unanimity  is  acquired  by  the  remaining  ideas.  They  pour 
in  upon  the  chairman  with  ever  greater  intensity.  He  is  set  into  activity  and  the  overwhelming 
idea  or  impulse  of  the  assembly  for  action  pours  through  him  to  his  Sheriff  and  Policemen: 
executives  who  correspond  to  the  groups  of  motor  nuclei  which  have  been  trained  by  previous 
reflex  and  voluntary  acts  to  execute  the  "will,"  of  the  individual,  which  is  really  the  dominant 
activity  of  his  cerebral  cortex. 

Speech  (Charts  IVc  and  XIII) 
The  most  complicated  and  important  of  all  voluntary  acts  is  speech.  Although  the  lower 
animals  can,  in  all  probability,  communicate  with  each  other,  speech  and  the  allied  functions, 
reading  and  writing,  are  peculiar  to  human  beings  and  are  the  result  of  much  instruction  in  the 
line  of  imitation  and  study.  These  functions,  therefore,  depend  upon  a  healthy  brain.  If  a  child 
has  such  an  imperfectly  formed  brain  that  he  is  an  idiot  (743),  he  consequently  cannot  speak. 
The  perfection  and  content  of  speech,  reading  and  writing  depend  upon  education;  being  more 
imperfect  the  less  the  education  and  training  and  are,  therefore,  often  quite  abnormal,  or  even 
absent,  in  the  defective  and  feeble-minded  (752,  1090,  1094)  and  in  hysteria  (747-8)  and  in- 
sanity, especially  in  adolescent  insanity  (1098),  in  dementia  (1079),  in  coma  (745)  and  in  in- 
sanity with  diffuse  cortical  changes  in  the  speech  area   (1106). 

The  power  of  speech  is  of  enormous  importance  in  the  development  of  the  race,  it  is  the 
one  factor  which  has  enabled  the  human  race  to  so  far  outstrip  all  other  animals  that  it  seems  to 
form  an  entirely  different  order  of  beings  from  them.  The  spoken,  and,  still  more,  the  written, 
word  allows  man  to  make  his  own  all  the  experience,  knowledge  and  wisdom  of  his  ancestors  and 
contemporaries,  and  raises  liim,  thus,  far  above  his  own  limited  individual  experiences. 

Like  all  knowledge,  the  art  of  speaking,  reading  and  writing  is  acquired  from  sensory  im- 
pressions. The  art  of  speech  is  not  in-born,  although  its  possibility,  its  meclianism,  is.  It 
is  derived  from  the  sense  of  hearing;  so  that  when  a  child  is  born  deaf,  or  ac- 
quires deafness  in  the  first  two  or  three  years  of  life,  he  is  also  dumb:  a  deaf  mute 
(744).  A  deaf  mute  can  be  taught  to  speak  only  very  imperfectly,  and  then  only  by  the  sense 
of  sight,  or  much  more  rarely  by  touch  (Helen  Keller).  The  art  of  reading  and  writing  is  de- 
rived partly  from  the  sense  of  hearing  and  mainly  from  the  sense  of  sight.  If  a  child  is  born 
blind,  or  acquires  blindness  in  the  first  few  years  of  life,  he  can  learn  to  read  only  books  printed 
in  a  peculiar  way,  and  then  only  by  the  sense  of  touch  and  hearing;  the  sense  of  touch  replacing 
the  sense  of  sight  in  these  cases. 

Many  persons  think  that  speech  comes  naturally,  or  by  nature,  to  a  child.  Such  is  not  the 
case.  In  a  home  and  hospital  for  infants  where  the  limited  number  of  nurses  were  so  busy  in 
attending  to  the  physical  needs  of  the  infants  that  they  had  little  time  for  anything  else,  it  was 
noted  with  some  .surprise  that  the  children,  grown  to  the  age  of  eighteen  months  and  two  years, 
made  no  effort  to  speak.  It  was  necessary  to  bring  in  some  older  girls  for  this  purpose  and  to  im- 
press on  the  nurses  the  necessity  of  devoting  attention  to  teaching  children  to  speak.  The  first 
sounds  which  the  child  utters,  little  cooing  sounds,  are  doubtless  emotional  reflexes,  scarcely 
more  complicated  than  laughing  or  crying.  From  the.se  sounds,  speech  is  gradually  built  up  by 
careful  training.  The  mother  in  her  play  with  the  child  imitates  these  sounds  and  gradually 
changes  them  into  so-called  "baby  talk :"  into  some  resemblance  to  actual  syllables  or  words.  The 

33 


child  who  is  continually  being  taught  to  imitate  the  mother,  very  slowly  changes  the  simple  coo- 
ing and  other  sounds  into  these  nearly  related  ones  and  finally  toward  the  end  of  the  first,  or  dur- 
ing the  second,  year  of  life.  Da-da  is  converted  into  pa-pa,  and  ma-ma,  and  other  simple  words.  It 
is  a  play  and  a  lesson  which  is  taking  place  every  day  in  every  nursery  in  the  land.  It  is  a  slow 
process,  but  after  a  time  the  child  begins  to  utter  words  to  which  he  at  first  attaches  no  signifi- 
cance or  understanding,  but  to  which  he  later  attaches  a  more  and  more  definite  meaning.  Thus, 
speech,  like  other  activities,  is  gradually  acquired    from  simple  reflex  acts. 

During  the  first  month  of  its  life  the  child  gives  utterance  only  to  vowel  sounds,  especially 
"oo"  and  "a."  Toward  the  end  of  the  second  month  he  begins  to  utter  consonants,  especially, 
"m"  and  "t,"  followed  in  the  third  month  by  "b"and  "g"  and  "r"  and  "n,"  and  in  the  fifth  month 
"k"  is  added.  During  the  second  half  of  the  first  year  the  child  holds  monologues,  as  if  really 
talking.  Some  of  the  sounds  can  be  represented  by  letters,  others  cannot.  He  shows  a  strong 
tendency  to  repeat  the  same  sound  over  and  over  and  over  again,  probably  in  part,  because  his 
vocabulary  of  sounds  is  not  large.  At  the  beginning  of  the  second  year  the  child  is  able  to  repeat 
with  some  accuracy  the  simplest  sounds  which  he  hears ;  but  even  when  he  learns  to  repeat,  with 
some  distinctness,  ."♦'mple  words  as  "mama"  and  "papa'"  he  attaches  at  first  no  meaning  to  them. 
At  the  same  time,  however,  he  is  beginning  to  understand  certain  words  that  are  said  to  him  and 
in  response  to  the  question,  "How  big  is  the  baby  ?"  he  raises  his  hands  to  approximately  the  level 
of  the  top  of  his  head.  Thus,  at  a  certain  stage  of  his  development  the  child  can  speak  words 
which  he  cannot  understand  and  can  understand  words  which  he  cannot  speak.  There  is  much 
doubt  as  to  really  how  much  he  understands.  The  raising  of  his  hands  may  be  a  conditioned 
reflex,  similar  to  those  already  described,  and  he  might  raise  his  hand  equally  well  to  the  words 
"How  small  is  the  baby?"  or  even  the  word  "big"  or  "ig"  or  even  to  inflection  of  the  voice  with- 
out any  spoken  word  at  all.  Thus  speech  is  at  first  a  modified  reflex.  After  this  process  has  gone 
on  for  a  time  the  child  acquires  a  great  facility  in  imitating  the  sound  of  words,  as  he  does  in 
all  kinds  of  imitation,  and  will  often  surprise  his  mother  by  uttering  a  sentence  wliich  he  has 
never  said  before,  although,  doubtless,  he  has  often  heard  it  said  by  others.  However  doubtful 
may  be  his  understanding  of  words  in  the  early  stages  of  this  process,  there  is  no  doubt  that  this 
understanding  is  slowly  acquired  and  finally  it  becomes  evident  that  the  child  clearly  associates 
an  object  with  a  definite  sound,  or  word.  He  often  points  to  an  object,  the  name  of  which  is 
spoken,  or  even  leads  one  to  it  when  he  is,  as  yet.  unable  to  walk  alone. 

It  is  evident  that  the  perceptions  and  memories  of  spoken  words  are  of  fundamental  import- 
ance in  the  art  of  spenking.  These  perceptions  take  place  and  these  memories  are  stored,  in 
right  handed  persons,  in  the  posterior  half  of  the  left  superior  temporal  convolution  and  in  the 
posterior  portion  of  the  left  island  of  Reil  (Fig.  15)  ;  so  that  lesions  of  this  area  cause  a  pro- 
found disorder  of  speech:  sensory  aphasia  (775-6).  From  this  portion  of  the  cortex  impulses  pass 
along  association  fibers  (the  fasciculus  uncinatus)  lying  in  the  external  capsule  to  the  base  of  the 
left  inferior  frontal  convolution  (Fig.  15)  and  to  the  anterior  portion  of  the  island  of  Reil.  A 
lesion  in  this  region,  also,  causes  a  profound  disorder  of  speech:  motor  aphasia  (774.) 

The  distinction  between  motor  and  sensory  aphasia  is  not  always  easily  drawn.  In  some 
cases  when  a  patient  is  unable  to  speak  a  desired  word  it  may  be  very  difificiilt  to  decide  whether 
he  has  forgotten  the  innervation  memories  necessary  to  speak  the  word  (motor  aphasia  — 222) 
or  has  forgotten  the  word  itself  (sensory  aphasia — 223).  In  the  latter  case  he  may  be  able  to 
repeat  the  word  when  he  hears  it  spoken.  Lesions  of  the  external  capsule,  in  which  run  the 
association  fibers  connecting  the  centers  of  sensory  and  motor  speech  (the  fasciculus  uncinatus). 
also,  cause  a  profound  disorder  of  speech  (conduction  aphasia). 

Perceptions  of  written  or  printed  words  are  formed  and  their  memories  are  stored,  in  right 
handed  persons,  in  the  cortex  of  the  left  occipital  lobe,  and  from  this  area  impulses  pass  along 
the  association  fibers  lying  beneath  the  angular  gyrus  to  the  base  of  the  left  inferior  frontal  con- 
volution and  the  base  of  the  loft  middle  frontal  convolution,  where  are  stored  the  innervation 
memories  of  speech  and  writing  respectively.  Therefore,  deep  lesions  in  the  region  of  the  left 
angular  gyrus  in  right  handed  persons  will  cause  a    complete  alexia     {ITJ^    and    an    incomplete 

34 


agraphia  (779).  The  area  of  the  cortex  in  the  left  hemisphere  described  above,  including  the 
bases  of  the  middle  and  the  inferior  frontal  convolutions,  the  island  of  Reil,  the  posterior  half  of 
tlie  superior  temporal  convolution  and  the  angular  gyrus,  is  called  "the  zone  of  language"  and  is 
the  cortical  center,  or  psychic  center,  for  the  faculty  of  language. 

In  addition  to  its  cortical  center,  speech  depends  upon  the  integrity  of  the  muscles  and  nerves 
which  move  the  lips,  tongue,  soft  palate,  larynx  and  those  concerned  in  respiration.  In  lesions  of 
these  muscles  and  nerves  and  of  their  nuclei  in  the  medulla  and  pons  and  of  the  pyramidal  tract, 
sp>eech  may  be  abolished  (anarthria)  or  pronunciation  impaired  (dysarthria),  whether  in  conse- 
quence of  paralysis  or  of  incoordination,  or  of  spasm  (as  in  stuttering).  Reading  and  writing 
may  be  similarly  abolished  or  impaired  in  lesions  of  the  peripheral  nerves  or  of  their  nuclei  in 
the  optic  thalamus  or  in  the  anterior  horns  of  the  cervical  enlargement  of  the  cord  or  of  the  fas- 
ciculus of  Gratiolet  or  of  the  pyramidal  tract. 

Dysarthria  might  also  be  due  to  a  cortical  tpajralysis  of  the  pneumogastric  nerve,  but  the 
laryngeal  muscles  have  a  bilateral  cortical  representation;  so  that  if  one  cortical  area  be  injured 
the  corresponding  area  of  the  other  hemisphere  can  carry  on  the  function  of  speech  perfectly. 
There  is,  therefore,  no  laryngeal  paralysis,  or  consequent  dysarthria,  due  to  any  lesion  within  the 
cerebral  hemispheres,  unless  the  lesion  be  very  extensive  and  involves  both  hemispheres 
(pseudo-bulbar  paralysis). 

Automatic   Movements  (Charts  III  and  XVI) 

This  term  is  applied  to  two  quite  different  sorts  of  actions.  In  one  sense  automatic,  or 
autochthonous,  acts  are  reflex  acts  which  originate ,  not  from  external,  but  from  internal,  or  or- 
ganic, excitations  or  irritations.  One  of  the  best  examples  of  this  activity  is  the  respiratory  act. 
Another  is  the  gastric  and  intestinal  peristalsis.  Such  acts  are  very  numerous  and  carry  on  the 
nutritive  activities  of  the  body. 

The  name  is  also  applied  to  voluntary  acts  which  have  been  learned  with  more  or  less  diffi- 
culty, but  which  have  been  enacted  so  often  that  ihey  can  be  performed  without  consciousness. 
Such  acts  are  walking,  writing,  piano-playing,  smoking  and  many  others  which  can  be  very  i>er- 
fectly  performed  unconsciously,  although  each  one  can  be  enacted  consciously  and  usually  is  so 
done.  The  nervous  impulses  underlying  these  automatic  acts,  although  they  may  be  entirely  un- 
conscious acts,  probably  always  pass  through  the  cerebral  cortex  and  are  never  shunted  to  the 
ganglia  at  the  base  of  the  brain.  Otherwise  it  is  hard  to  understand  why  in  destructive  lesions  of 
the  motor  cortex,  the  corona  radiata,  or  the  internal  capsule  these  automatic  acts  are  abolished,  as 
they  surely  are. 

Involuntary   and   Abnormal  Motor  Responses 

Spasms  and  Couz'iilsions  (Chart  IVb).  Spasms  and  convulsions  consist  in  involuntary 
muscular  contraction.  They  depend  mainly  upon  irritation  of  the  central  gray  matter,  especially  the 
cerebral  cortex,  and  partly  upon  peripheral  irritation. 

Passive  contracture  and  Thomsen's  disease  alone  are  purely  of  peripheral  (muscular)  on- 
gin.  Many  of  the  tonic  spasms  are  reflex,  some  are  the  result  of  nerve  root  irritation  (menin- 
gitis, tumors,  etc.)   and  many  are  associated  with  degeneration  of  the  pyramidal  tracts. 

The  result  of  pathological  and  experimental  investigation  makes  it  evident  that  epileptic 
and  epileptiform  convulsions  may  originate  from  irritation  of  the  motor  cortex.  When  a  slight, 
but  lasting,  local  irritation  of  the  motor  cortex  occurs,  there  results  a  local  spasm,  clonic  and 
tonic,  which  extends  from  one  extremity  to  another  and  finally  becomes  a  general  convulsion, 
accompanied  in  some  cases  by  coma.  When  the  irritation  is  stronger  and  especially  when  it 
affects  both  hemispheres  there  results  first  a  tonic  followed  by  a  clonic  convulsion  and  coma. 
Irritation  of  other  parts  of  the  cortex  can  also  produce  epileptic  convulsions,  if  the  irritation  be 
strong  enough  and  the  motor  cortex  be  intact.  Tonic  spasms,  without  clonic  ones,  may  be  ob- 
tained by  irritation  of  many  parts  of  the  central  nervous  system.  The  epileptiform  convulsion 
caused  bv  cortical  irritation  may  be  accompanied  by  alterations  in  the  cardiac  action,  in  the  respira- 

35 


tion  and  in  the  activity  of  other  internal  organs,  as  in  the  cases  of  ordinary  epilepsy.  Indeed, 
these  changes  in  the  cardiac  action  and  in  the  circulation  through  the  brain  may  be  more  essential 
factors  than  is  the  cortical  irritation  in  the  production  of  some  of  the  symptoms  of  an  epileptic 
attack. 

The  contractures  which  accompany  cerebral  paralyses  are  due  to  contraction  of  the  stronger 
muscles,  partly  in  efforts  for  voluntary  movements  from  the  brain,  but  mainly  reflexly  from  the 
spinal  cord. 

The  pathogenesis  of  many  spasms  and  the  localization  of  their  origin,  especially  of  the  ir- 
regular spasm,  are  given  in  Chart  IVb. 

The  various  forms  of  spasms  are  at  times  quite  difficult  to  recognize.  It  requires  much 
experience  to  be  able  always  to  differentiate  clonus,  tics,  athetoid  and  choreic  spasms  from  one 
another  and  from  the  perversions  of  motion:  tremor,  ataxia  and  apraxia.  Tliis  is  imfortunate 
because  the  diagnosis  by  these  diagnostic  charts  requires  that  the  symptoms  be  correctly  observed 
and  named.  The  student  should  compare  carefully  what  he  sees  with  the  definitions  in  the  book 
and  should  observe  as  many  cases  as  possible. 

Ataxia,  Apraxia  and  Tremor  {Chart  IV c).  When  an  impulse  from  a  cortical  motor  center 
passes  down  to  a  group  of  nerve  cells  in  the  anterior  horns  of  the  spinal  cord,  it  causes  a 
definite  synergic  contraction  of  a  number  of  muscles  to  produce  the  movements  over  which  the 
group  of  nerve  cells  presides.  As  soon  as  this  movement  commences,  a  number  of  sensory  im- 
pulses pass  from  the  muscles  and  joints  involved  to  the  coordinating  centers,  especially  to  the 
cerebellum,  and  the  movement  is  consequently  coordinated  and  orderly.  This  coordination 
of  movements  is  not  inborn.  It  is  acquired  by  experience  and  practice.  The  movements  of  a 
new  bom  baby  are  always  ataxic.  When  the  function  of  the  cortical  center  is  impaired  there 
results  a  paralysis  or  an  apraxia  (loss  of  skill)  according  to  the  degree  of  the  impairment  and 
when  the  coordinating  apparatus  is  functionally  impaired  there  results  ataxia.  In  either  rase 
awkward,  ill-adapted  and  uncertain  movements  result.  In  cerebellar  lesions  there  is  asynergy: 
the  muscles  taking  part  in  the  movement  do  not  act  together  at  the  proper  time  and  with  the 
proper  relative  force  to  produce  an  orderly  movement. 

The  motor  apparatus,  together  with  its  sensory  regulation,  may  be  called  the  executive 
apparatus  and  it  may  be  disordered  in  various  ways: 

1st.  If  the  motor  portion  of  this  apparatus  be  injured  there  results  a  paralysis  or  paresis. 
See  Chart  IVa. 

2nd.  If  the  sensory  or  regulating  apparatus  be  injured  there  results  ataxia.  See  Chart 
IVc. 

3rd.  If  what  has  been  learned  has  been  lost  or  impaired  there  results  apraxia  or  dyspraxia. 
See  Chart  IVc. 

Ataxia,  incoordination  of  movement,  always  depends  upon  .some  disturbance  of  the  sen- 
sory or  regulating  apparatus.  It  occurs  in  several  distinct  varieties,  depending  upon  the  portion 
of  the  sensory  nervous  system  afifected : 

1st.     Peripheral,  or  dynamic,  due  to  lesion  of   the   peripheral    sensory   neurons. 

2nd.  Cerebellar,  or  static,  due  to  lesion  of  the  cerebellum  or  its  tracts,  including  the  termin- 
nation  of  the  auditory  nerve  in  the  semi-circular  canals. 

3rd.     Cerebral  ataxia,  to  a  lesion  of  the  cerebral  hemispheres. 

1.  Peripheral,  or  dynamic,  ataxia  (280,  644)  is  caused  by  an  impairment  or  loss  of  the 
complicated  sensations  conveyed  by  sensory  fibers  from  the  muscles,  joints  and  other  tissues 
which  is  known  by  the  name  of  muscle-joint  sense  (43  and  352).  It  affects  all  movements  of  the 
parts  involved.  It  is  associated  with  hypotonia  (240),  which  allows  an  abnomial  excursion  in 
passive  movements  without  the  resistance  normally  offered  under  sudden  stretching,  and  which 
may  allow  of  abnormal  positions  of  the  extremities.  The  loss  of  the  muscle-joint  sense  can  to 
some  extent  be  replaced  by  the  sense  of  sight,  which  allows  the  patient  to  guide  his  movements 
by  his  eyes. 

Cerebellar,  or  static,  ata.via  (281,  642)  is  caused  by  impairment  of  the  function  of  the  great 
coordinating  organ :     the  cerebellum.       It  affects  mainly,  or  only,  walking  and  standing,  wliich  acts 

36 


resemble  those  of  a  drunken  man,  or  become  absolutely  impossible.  The  sense  of  sight  gives 
very  little  aid  in  such  cases.  Movements  of  the  extremities  while  the  patient  is  recumbent  are 
fairly  normal.  With  cerebellar  ataxia  is  usually  associated  vertigo;  although  this  latter  symptom 
may  not  be  pronounced. 

Cerebral  ataxia  is  due  to  a  lesion  of  the  sensory  tracts  and  centers  within  the  brain.  If 
this  lesion  involves  the  sensory  tracts  in  the  medulla  or  pons  or  crura  cerebri,  the  cerebellar 
tracts  may  also  be  involved  and  the  ataxia  may  be  either  cerebellar  or  dynamic  or  both.  In 
cases  of  cerebral  hemianesthesia  where  the  lesion  is  either  in  the  optic  thalamus,  the  internal 
capsule  or  the  parietal  cortex,  the  ataxia,  which  invariably  results,  is  of  the  dynamic  variety  and 
is  associated  with  hypotonia.  Such  cases  of  ataxia  may  be  slight  in  degree  and  may  show  great 
and  relatively  rapid  improvement.  When  the  lesion  is  in  the  parietal  cortex,  the  center  for 
cutaneous  and  muscular  sensibility,  ataxia  results,  because  of  the  loss  of  those  sensations  wliich 
are  essential  for  the  proper  guidance  of  voluntary  movements.  In  tumors  of  the  frontal  lobe, 
whether  cortical  or  sub-cortical,  ataxia  is  a  common  symptom  and  is  of  the  cerebellar  type;  being 
doubtless  due  to  involvement  of  the  fronto-cerebellar  tract.  In  cerebral  ataxia,  it  is  evident  that 
the  patient  is  trying  to  execute  the  movements  and  knows  what  he  wants  to  do,  but  he  executes 
them  awkwardly. 

Apraxia  (282)  may  residt  from  the  loss  of  the  purposeful  idea  which  should  prompt  a  given 
action.  In  lesions  of  the  posterior  central  convolution  or  of  the  supra-marginal  gyrus  this  idea 
cannot  be  formed  (sensorial  apraxia  or  agnosia),  in  which  case  the  action  which  should  follow 
the  idea  cannot  originate;  or  when  this  idea  is  formed  the  memory  is  quickly  lost  (amnestic 
apraxia),  in  which  case  the  appropriate  action  is  begun,  but  never  completed.  In  lesions  of  the 
anterior  central  convolution,  or  of  the  area  immediately  anterior  to  it,  the  purposeful  idea  may 
be  present,  but  the  innervation  memories  necessary  for  the  production  of  the  appropriate  action 
are  lost;  so  that  the  action  cannot  be  performed  (motor  apraxia).  When  the  association  fibers 
connecting  the  anterior  and  posterior  central  convolutions  are  the  seat  of  lesions,  the  appropriate 
action  will  not  occur,  or  a  somewhat  similar  action  may  be  substituted  for  it  (associative  apraxia). 

In  any  organized  society  much  results  from  imitation  and  from  instruction.  Certain 
complexes  of  innervation  feelings  become  by  practice  so  firmly  united,  that  what  was  at  first 
done  with  difficulty  and  imperfectly,  becomes  easily  and  perfectly  performed.  These  innervation 
complexes  are  not  inborn  (although  their  anatomical  substructure  may  well  be),  but  are  learned 
and  acquired  by  practice.  These  innervation  complexes  become  memories  (kinesthetic  mem- 
ories). Innervation  memories  may  be  conscious  in  early  life  when  first  learned,  but  may  be 
unconscious  later.  Many  of  them  may  never  enter  consciousness.  As  long  as  these  memories 
persist  the  corresponding  action  may  be  performed,  consciously  or  unconsciously,  as  the  final 
result  of  sensory  impulses  exciting  them.  Many  complicated  acts  are  not  performed  often 
enough  to  form  an  innervation  complex,  but  must  be  performed  consciously  and  with  constant 
sensory  guidance  from  many  parts  of  the  brain  simultaneously   (sight,  muscle  sense,  touch,  etc.). 

Tremor  (250)  may  be  caused  by  rapid  rhythmical  interruptions  of  the  inner\-ation  impulses 
passing  to  the  muscles  or  by  failure  of  a  proper  proportion  or  equilibrium  in  the  innen-ation 
of  the  muscles  and  their  antagonists,  and  is  especially  characteristic  of  lesions  of  the  lenticular 
nucleus  and  of  the  red  nucleus  and  rubro-spinal  tract.  Tremor  usually  ceases  during  sleep  and  is 
usually  increased  by  mental  excitement;  although  a  very  powerful  emotion  may  arrest  the  tremor 
temporarily.  It  seems  to  be  always  of  central  origin.  Clonic  spasm  from  exaggerated  reflexes 
must  not  be  confounded  with  a  coarse  tremor. 

Athetosis,  or  mobile  spasm,  is  a  slow  twisting  movement  of  the  fingers  and  hands,  either  uni- 
lateral or  bilateral.  It  often  follows  a  hemiplegia  or  diplegia,  and  occurs  most  frequently  in 
cerebral  palsy  of  childhood.  It  is  characteristic  of  lesions  of  the  caudate  nucleus  and  of  the 
putamen. 

Trophic  Influences   (Chart  XVII) 

The  nervous  system  exercises  an  important  trophic  influence  over  many  of  the  tissues  of 
the  body,  in   addition  to  influences  over  their  blood     supply     through    the    vaso-motor    system. 

37 


This  trophic  influence  can  be  divided  into  two  great  divisions,  motor  and  sensory.  When  the 
motor  nerve  cells  of  the  central  or  peripheral  motor  neurons  are  degenerated  or  destroyed  (as 
in  lesions  of  the  nerve  fibers  or  of  the  motor  cells,  of  which  these  nerve  fibers  are  the  axons), 
the  nerve  fibers  springing  from  such  degenerated  cells  undergo  a  rapid  degeneration,  as  do  also 
the  muscles,  in  which  these  nerve  fibers  terminate ;  and  in  early  life  when  there  is  motor  paralysis, 
or  immobilit)'  of  parts  of  the  body  from  any  cause,  these  parts  fail  to  grow  normally. 

When  the  sensory  nerves  are  degenerated,  as  in  syringomyelia,  myelitis,  tabes,  lesions  of 
the  spinal  ganglia  or  of  the  ganglia  at  the  ba9e  of  the  brain,  etc.,  in  consequence  of  the  anes- 
tliesia  thereby  produced,  the  body  is  no  longer  protected,  by  reflex  and  voluntary  acts,  from  the 
many  traumatisms  to  which  it  is  frequently  subjected  and  therefore  ulcerations,  arthropathies,  ul- 
cerations of  the  cornea  and  other  tropliic  lesions  result. 

Some  of  the  ductless  glands,  especially  the  pituitary  and  the  thyroid,  when  hypertrophied 
or  atrophied  as  regards  their  glandular  structure,  also  produce  widespread  trophic  disorders. 

The  Cerebro-Spinal  Fluid   (Charts  VIII  and  XIX) 

The  central  nervous  organs  (brain  and  spinal  cord)  are  bathed  in  a  fluid  called  the  cerebro- 
spinal fluid.  This  fluid  is  secreted  or  transudes  from  the  choroid  plexus  within  the  ventricles 
of  the  brain  and  thus  may  contain  substances  which  are  in  the  blood.  It  passes  out  of  the 
ventricles  at  the  inferior  angle  of  the  fourth  ventricle,  through  the  foramen  of  Magendie.  If 
from  any  cause  (tumor,  meningitis,  etc.)  the  foramen  of  Magendie  is  occluded,  this  fluid,  con- 
stantly secreted,  cannot  escape  from  the  ventricles  and  dilates  these  cavities  more  or  less  ac- 
cording as  the  sutures  of  the  skull  are  ossified  less  or  more  completely ;  thus  producing  internal 
hydrocephalus.  The  cerebro-spinal  fluid  passing  out  of  the  foramen  of  Magendie  becomes  the 
subarachnoid  fluid,  which  lies  in  the  meshes  of  the  tissue  forming  the  deeper  layers  of  the 
arachnoid.  In  this  situation  it  can  receive  products  of  any  inflammation  of  the  meninges : 
albuminous  substances  (globulin)  and  cellular  structures  (leucocvtes  in  acute,  and  lymphocytes 
in  chronic,  inflammations)  ;  so  much  so  as  to  be  cloudy  or  even  purulent.  The  specific  germs 
of  the  various  forms  of  meningitis  can  often  also  be  detected,  as  well  as  blood  in  hemorrhage 
and  pus  in  abscess.  In  tertiary  and  quaternary  syphilitic  meningitis  the  Wassennann  reaction 
is  usually  positive.  The  cerebro-spinal  fluid  leaves  the  cranial  and  vertebral  cavities  along  the 
cranial  and  spinal  nerves  and  through  the  Pacchionian  bodies  and  enters  the  veins. 

The  cerebro-spinal  fluid  is  obtained  by  lumbar  puncture  and  the  rapidity  of  its  escape  is 
evidence  of  the  tension  which  it  is  under,  which  tension  c"an  more  accurately  be  measured  by 
a  manometer.  When  the  cerebro-spinal  fluid  is  increased  in  amount,  as  in  meningitis,  or  when 
a  foreign  body,  as  a  tumor,  is  within  the  cranial  or  spinal  cavity  the  tension  of  the  fluid  is  usually 
increased.  The  examination  of  this  fluid  is,  therefore,  of  much  importance  in  disease  of  the 
cerebral  and  spinal  meninges  and  in  other  intra-cranial  and  intra-spinal  conditions. 

Electricity  and  the  Nervous  System  (Chart  II) 

Nervous  conduction,  although  it  has  some  analogies  with  electrical  conduction,  is  due  to  an 
entirely  difl^erent  form  of  energy.  But  when  nervous  action  takes  place,  whether  in  a  peri- 
pheral nerve  or  in  a  central  ganglion,  there  always  occurs  an  electrical  current  through  the  nerve 
or  ganglion  in  the  opposite  direction.  So  constant  and  delicate  is  this  reaction,  that  it  has  been 
used  to  prove  the  presence  of  nervous  activity.  Moreover  the  electric  current,  both  Galvanic 
and  Faradic,  can  be  conducted  along  nerve  fibers,  and  changes  in  the  tension  of  electricity  so  con- 
ducted in  the  nerve  fibers  cause  contraction  of  the  muscles  in  which  they  terminate,  as  is  shown  in 
Oiart  VII.  The  muscle  fibers,  also,  respond  directlv  to  changes  in  intensity  of  a  Gal- 
vanic current,  but  not  to  those  of  a  Faradic  current.  Degeneration  of  a  nerve  can  be  shown  by 
its  reactions  to  electricity  C Chart  VI lb). 

All  forms  of  electrical  energy  are  excitants  for  all  the  sensory  organs,  acting  not  so  much 
upon  the  end-organs  as  upon  the  nerves  themselves. 

Other  forms  of  electricity,  especially  static  electricity  and  high  frequency  currents,  are 
used  as  therapeutic  measures  but  have  no  diagnostic  value. 

38 


CHART  I 

Case-Taking 


METHODS  OF  EXAMINATION  OF  PATIENTS     SUFFERING     FROM     NERVOUS 

DISEASES.  teisS^^;.^...  / 

Errors  in  diagnosis  result  more  frequently  from    imperfect    observation    than    from    faulty 
reasoning. 


Methods  of  Examining  and  Testing 
Patients 


Data  derived  from 

QUESTIONING 

INSPECTION 

PALPATION 

PERCUSSION 
^  ELECTRICITY 

LUMBAR  AND  BRAIN  PUNCTURE 

OPHTHALMOSCOPY 

LARYNGOSCOPY 
L  THERMOMETRY 


see  chart  I  a. 
see  chart  I  b. 

see  chart  I  c. 


.  see  chart  I  d. 


39 


CHART  la 

Questioning 

Comprising  Numbers  1  to  18 

(Note) — The  examination  of  every  patient,  who  is  conscious  and  intelligent,  begins  with 
a  history  of  his  health  and  of  that  of  his  ancestors.  This  is  an  important  source  of  information, 
although  usually  less  so  than  are  the  results  of  the  physical  examination.  The  taking  of  a 
reliable  clinical  history  is  something  of  an  art,  but  at  best  we  are  absolutely  dependent  upon 
the  truthfulness  of  the  patient,  as  we  rarely  have  means  to  check  his  statements  by  informa- 
tion from  other  sources.  It  is  important  to  put  the  patient  at  his  ease  and  to  gain  his  confidence. 
The  patient  is  vitally  interested  in  his  own  case  and  it  is  best  to  let  him  tell  his  own  story  of 
his  illness  in  his  own  way,  without  interruption.  He  is  eager  to  tell  of  his  personal  sufiferings  Jind 
often  becomes  impatient  and  irritable  if  interrupted  by  questions  as  to  his  hereditary  and  previous 
illness,  which  may  better  be  asked  later.  When  he  has  finished  his  own  story  is  the  time  to  ques- 
tion him  about  his  illness,  more  especially  and  fully  in  regard  to  the  organ  probably  affected,  but 
also  concerning  the  function  of  the  other  organs  of  the  body.  This  done,  he  should  be  questioned 
as  to  his  previous  illnesses,  occupations,  etc.,  and  finally  as  to  any  special  prevailing  illness  in  his 
ancestors  or  relatives.  It  is  important  to  ask  as  few  leading  questions  as  possible.  Questions 
in  regard  to  personal  habits  and  venereal  diseases  should  only  be  asked  when  absolutely  alone  with 
the  patient,  and  then  in  a  manner  wliich  assumes  that  all  men  are  guilty  of  indiscretions.  During 
our  taking  of  the  clinical  history  we  should  have  the  patient  under  close  observation  and  can 
thus  form  a  good  judgment  as  to  his  manner  and  general   mental  and  physical  characteristics. 


41 


Methods  of  Examination  of  Patients  Suffering  from  Nenous  Diseases 


QUESTIONING 
Methods  of  Testing 

11  Allow  the  patient  to  tell  the  story  of  the  illness  without  interruption  (see  note  on 

History  of  pres-  preceding  page).  Then  ascertain  the  exact  date  and  manner  of  onset  (sudden 
or  slow,  prodromata,  etc.)  and  tlie  exact  sequence  of  symptoms.  Inquire  into 
all  details  which  may  concern  the  case  (headache,  pain,  paresthesiae,  vertigo,  in- 
somnia, mental  condition,  emotions,  memory,  special  senses,  paralyses,  spasms, 
fits,  disturbances  of  organic  reflexes,  loss  of  weight  and  strength,  etc. ),  whether 
of  recent  or  of  old  date.  Seek  for  any  possible  cause  (injury,  poisons,  drugs, 
infections,  worry,  mental  or  physical  overstrain,  shock,  etc.).  Be  careful  not 
to  suggest  answers  to  nervous  people.  Inquire  into  previous  treatment  and  its 
effect. 


ent   illness. 
(Chart   II) 


Family  and 
personal 
history. 

(Chart  II) 


3 

Consciou 
( Charts 
XVI) 


sness. 
Ill   & 


4 

Sanity. 
(Charts 
XVI) 


III  & 


.\scertain  the  occurrence  in  the  present,  or  a  past,  generation  of  the  family  of 
consanguineous  marria-ges,  of  any  nervous  diseases,  especially  the  neuroses 
(neuralgia,  epilepsy,  hysteria,  insanity,  suicide,  dnmkenness,  etc.),  or  of  sypliilis 
or  tuberculosis.  Note  patient's  age,  full  address,  race,  his  mental  and  physical 
development,  his  school  life,  injuries  at  birth,  occupation,  habits  (alcohol, 
drugs,  venery,  masturbation,  etc.),  exhaustion,  anxiety,  worry,  dwelling  and 
previous  illness,  such  as  rickets,  infectious  diseases,  chorea,  fits,  tuberculosis, 
syphilis  (use  discretion  in  this  inquiry:  ask  of  women,  about  sore  throat,  skin 
rashes,  miscarriages,  etc.,  and,  for  men,  a  good  question  is:  "Of  course,  like  all 
the  rest  of  us  you  have  had  the  clap.  Have  you  ever  had  the  pox  or  any  sore 
on  the  genitals?")  This  may  make  confession  easier.  Ascertain  the  condition 
of  other  organs  (cancer  and  tuberculosis). 

Psychoanalysis  is  a  part  of  the  personal  history.  It  is  a  minute  and  exhaustive 
inquiry  into  the  patient's  previous  and  present  actions,  motives  and  dreams, 
especially  in  regard  to  unhappy  and  repressive  influences  in  the  sexual  life,  of 
which  the  patient  is  scarcely,  if  at  all,  conscious  and  which  have  been  repressed 
rather  involuntarily  than  deliberately.  The  repressed  idea  may  express  and 
reveal  itself  (to  a  skilled  investigator)  in  dreams,  symbols,  phobias,  etc.  Psy- 
choanalysis and  its  concomitant  treatment  may  produce  in  some  cases  beneficial 
results,  but  equally  good  results  may  follow  other  treatment  and  the  method, 
fascinating  though  it  be,  seems  to  the  author  to  be  fraught  vdth  danger  and  is 
not  recommended. 

Patient  may  lie  in  a  stupor  and  make  little  or  no  response  to  questions,  noises, 
shaking,  pin  pricks,  or  strong  sensory  irritations  of  any  kind.  He  may  appre- 
ciate neither  his  surroundings,  nor  his  acts,  nor  the  time  and  place,  nor  his 
own  individuality.  He  can  remember,  after  recovery,  nothing  of  what  hap- 
pened while  he  was  uncon.scious.  There  are  all  possible  grades  in  impairment  of 
consciousness  from  complete  coma  to  a  slight  lack  of  attention  and  an  inability 
to  collect  one's  thoughts.     This  can  he  learned  by  conversation. 

Patient's  conversation  and  manner  may  show  that  his  brain  acts  in  an  abnormal 
way  and  that  he  entertains  abnormal  perceptions  and  ideas  (hallucinations, 
delusions,  compulsory  acts,  ideas,  etc.).  Ascertain  if  a  change  has  taken 
place  in  the  patient's  normal  mental  state,  and  when.  Note  whether  patient 
is  elated,  active,  loquacious;  or  dull,  inattentive,  sluggish,  distracted,  evasive, 
suspicious,  and  why.  Some  cases  may  require  prolonged  observation.  At 
times  irritating  questions  may  be  desirable,  in  order  to  evcile  the  patient. 


A2 


]  ntelligence. 
(Charts   III, 
XIII  &  XVI) 


Memory   and 
under- 
standing. 

(Charts  III, 
XIII  &  XVI) 


Emotions. 
(Charts  III  & 
XVI) 


8 

Speech. 
(Charts  III, 

XIII  & 

XVI) 


9 

Reading. 
(Charts  III, 

XIII  & 

XVI) 

10 

Writing. 
(Charts  III, 

XIII   & 

XVI) 

11 

Stereognosis. 
(Charts   III, 

VI  & 

XXII) 


QUESTIONING  (Continued) 

In  testing  a  patient's  intelligence,  we  test  his  general  knowledge  by  asking  him 
to  name  the  ditiferent  days  aiad  the  different  months  and  by  arithmetical,  geo- 
graphical, political  and  historical  questions.  His  power  of  observation  by  show- 
ing him  a  number  of  things  and  asking  him  later  to  describe  them.  His  poti^er 
of  attention  by  asking  him  to  add  a  long  column  of  figures  or  underscore  a  letter 
wherever  it  occurs  in  a  page  of  print.  His  pozver  of  comprehension  by  asking 
him  to  e-xplain  something  he  has  read  or  heard.  His  association  of  ideas  by 
giving  him  a  word  and  asking  what  other  ideas  it  suggests  to  liim.  His  mental 
reaction  time  by  the  time  he  takes  to  solve  problems,  or  to  name  an  object,  the 
picture  of  which  is  shown  to  him.     His  moral  sense  by  questions  in  ethics. 

.'\n  apparent  defect  in  intelligence  may  be  due  to  lack  of  attention,  or  may  be 
shown,  by  further  questioning,  by  having  him  repeat  long  phrases,  execute 
verbal  and  written  commands  and  name  objects  shown  to  him,  to  be  due  wholly, 
or  in  part,  to  a  loss  of  memory;  either  general  (amnesia),  or  local  (aphasia), 
especially  to  a  failure  to  understand  what  is  said  to  him  (sensory  aphasia)  ; 
while  reason  and  judgment  are  normal.  Test  memory  for  remote,  as  well  as 
for  recent,  occurrences.  Test  memory  of  statements  made  a  few  minutes 
previously,  or  of  events  of  the  day  before,  or  of  years  before. 

Patients  may  show  by  their  conversation,  if  suitably  guided,  or  by  their  manner, 
or  by  both,  whether  they  are  emotional  or  not.  The  emotional  state  of  the 
patient  and  the  mental  characteristics  discussed  just  above,  can  often  best  be 
learned  from  the  statements  of  friends  and  relatives.  Curious  fears,  the  so- 
called  "phobias,"  (235)  are  often  present. 

Patients's  speech  may  be  entirely  absent  (anarthria)  or  altered  and  very  defec- 
tive, rational  or  irrational ;  there  may  be  a  limited  vocabulary  or  use  of  the 
wrong  word  (aphasia),  poor  articulation  (dysarthria),  tremor  in  voice,  monot- 
onous, scanning  speech,  omissions  of  syllables  and  words,  and  may  show  indi- 
vidual peculiarities,  all  of  wliich  are  to  be  noted.  Speech  is  tested  by  interro- 
gation and  spontaneous  (voluntary)  speech.  Test  also  patient's  understanding 
of  letters,  words  and  phrases  spoken  to  him,  his  executing  spoken  and  written 
commands,  his  picking  out  objects  named;  and  have  patient  name  objects,  give 
sequences,  i.  e..  numbers,  days  of  week,  months,  etc.,  and  repeat  catch  phrases, 
as  "Round  the  rough  and  rugged  rock  the  ragged  rascal  ran,"  etc. 

Ask  the  patient  to  read  aloud,  even  short  sentences,  words,  or  letters  only  If  this 
be  impossible  can  he  read  to  himself?  Can  he  recite,  can  he  understand  what 
he  has  read?     Can  he  execute  written  commands? 

Ask  the  patient  to  write,  spontaneously,  from  dictation  and  from  copy.  Have 
him  write  the  names  of  objects  shown  him.  Note  any  defect  in  the  character 
of  the  writing  or  in  the  ideas  expressed.  Can  he  read  and  understand  what  he 
has  written  ? 

.^sk  the  patient  to  name  objects  placed  in  his  hand,  his  eyes  being  shut,  after 
excluding  anesthesia.  Even  without  feeling  them  all  over  and  without  moving 
them  about  in  his  fingers,  a  normal  person  should  be  able  to  recognize  many 
objects  (metals,  cloth,  etc.)  merely  laid  against  the  skin  of  his  hand,  face,  foot, 
lips,  etc.  Stereognosis  may,  therefore,  in  exceptional  conditions,  be  tested, 
although  less  perfectly,  in  other  parts  than  the  hands. 


43 


12 

Sight. 

(Charts  VI  & 
XIV) 


13 

Achromatopsia. 
Color  sense. 
(Chart  VI) 

14 

Field  of  vision 

for  white 

and  colors. 
(Hemiano- 

pia) 
(Qiarts  VI 

&  XIV) 


15 

Hearing  and 

tinnitus 
aurium. 
(Charts  VI  & 

XIV) 


16 

Smell. 

(Charts  VI  & 
XIV) 

17 

Taste. 

(Charts  VI  & 
XIV) 

18 
Slec->. 


QUESTIONING   (Concluded) 

Ask  the  patient  to  read  small  print  or  Jaeger's  test  type  at  reading  distance  (10 
to  16  inches,  according  to  age,  refractive  conditions,  etc.)  and  Snellen's  test 
letters  at  twenty  feet.  If  patient  cannot  read  the  appropriate  line  at  twenty 
feet  the  loss  of  vision  is  expressed  by  the  number  of  feet  from  the  chart  at 
which  he  can  read  this  line  divided  by  twenty.  Thus  at  ten  feet  the  vision 
would  be  expressed  by  -.^-  In  great  defect  of  vision  the  patient  may  be  able 
to  see  only  dimly  the  hand  moved  before  his  eye,  or  may  only  be  able  to  dis- 
tinguish between  light  and  darkness.  In  testing  suspected  malingerers,  who  claim 
to  be  blind  in  one  eye,  while  testing  the  sight  with  plain  or  low-power  lenses, 
both  eyes  being  open,  a  greatly  over-correcting  high-power  lens  should  be  surrep- 
titiously placed  before  the  normal  eye.  Then,  if  he  can  read  the  test-type,  he 
must  do  so  with  the  eye  which  he  claims  to  be  blind. 

Ask  the  patient  to  match  different  colored  worsteds  of  various  shades  by  day  light. 
Color  blindness  may  also  be  detected,  and  perhaps  more  accurately,  in  a  dark 
room  with  a  lantern  with  colored  glass. 

Place  the  patient  with  back  to  the  window  or  light  and  have  him  close  his  left 
eye  and  with  his  right  gaze  at  the  observer's  left  eye.  Then  let  the  observer 
move  his  hajids  about  in  a  plane  mid-way  between  himself  and  the  patient; 
so  that  each  should  see  the  hand  at  the  same  instant  as  it  comes  into  the  field 
of  vision.  The  observer  can  see  if  the  patient's  eye  wanders  from  his  own  and 
recall  it.  Test  left  eye  in  same  way.  If  any  defect  in  field  of  vision  is  suspected, 
use  a  perimeter.  With  a  perimeter  not  only  the  field  of  vision,  but  also,  by 
using  different  colored  papers,  the  color  field  can  be  mapped  out.  Normally 
the  color  field  is  largest  for  blue,  then  for  yellow,  orange,  red,  green,  etc.,  in 
the  order  named.  If  tliis  order  is  changed  there  is  said  to  be  an  "inversion  of 
the  cloror  fields"  (851-2).  Normally  the  lines  limiting  the  different  color  fields, 
when  charted,  are  everywhere  separate  from  each  other.  If  they  touch  or  cross 
there  is  "interlacing  of  the  color  fields"  or  "dychromatopsia"  (851-2). 

The  patient's  hearing  may  be  tested  by  voice,  watch,  or  tuning  fork.  Be  sure 
there  is  no  wax  in  the  ear.  Ascertain  whether  he  understands  what  is  said  to 
him,  i.  e.,  executes  spoken  commands.  Galton's  whistle  should  be  used  for  test- 
ing high  and  low  notes.  Each  ear  should  be  tested  separately.  Bone  conduc- 
tion is  tested  by  holding  watch  or  tuning  fork  firmly  on  skull.  Normally  a  tun- 
ing fork,  which,  held  on  mastoid  ceases  to  be  heard,  can  still  be  heard  when  held 
close  to  meatus  (Rinne's  test).  Normally  a  vibrating  tuning  fork,  held  on 
center  of  forehead,  is  heard  equally  in  both  ears.  If  heard  best  in  the  deaf 
ear  (positive)  the  lesion  is  in  external  or  middle  ear.  If  heard  best  in  the  nor- 
mal ear  (negative)  the  lesion  is  in  inner  ear  or  in  auditory  nerve  (Weber's 
test).  We  also  ask  about  ringing  in  ears  (tinnitus  aurium).  In  testing  a  malin- 
gerer, who  claims  to  be  deaf  in  one  ear,  place  in  his  ears  the  ear-pieces  of  a 
stethoscope  with  long  rubber,  not  metallic,  tubes  and  speak  into  the  bell  (chest- 
piece)  held  some  distance  behind  his  back.  While  so  speaking  compress  first 
one  then  the  other  tube  a  ntmiher  of  times.  It  will  soon  be  evident  whether  he 
can  hear  with  each  ear,  since  he  cannot  tell  which  tube  is  open  and  which  is  shut. 

Ask  the  patient  to  name  from  its  odor  any  fragrant  substance  (such  as  asafoetida, 
cloves,  peppermint,  etc.)  held  for  a  moment  beneath  each  nostril  in  turn,  the 
other  being  closed.     Ammonia  and  acetic  acid  should  not  be  used  in  this  test. 

Ask  the  patient  to  point  to  the  name  on  a  printed  card  of  the  taste  of  a  strongly 
bitter,  sweet,  salt  or  sour  solution  touched  from  a  medicine  dropper,  or  a 
camel's  hair  brash,  to  one  side  after  the  other  of  the  protruded  tongue.  The 
tongue  should  be  well  washed  between  each  test. 

The  amoimt  of  sleep  which  the  patient  gets  in  the  twenty-four  hours  is  always 
an  important  question.  Insomnia  fagrypnia)  is  present  in  many  nervous 
diseases  and  is  apt  to  be  exaggerated  by  patients;  so  that  their  statements  should 
be  controlled,  when  possible,  by  those  of  the  nurses  or  relatives.  Many  symp- 
toms, especially  fears,  are  worse  at  night:  "Pavor  noctumus  of  children." 


44 


CHART  lb 
Inspection  (mainly) 

Comprising  Numbers  20  to  43. 


45 


Methods  of  Examination  cf  Patients  Suffering  from  Nervous  Diseases 


20 

Facial    expres- 
sion and  gen- 
eral   appear- 
ance and 
behavior. 

(Charts  XVI 
&  XVII) 


21 

Walk. 
(Chart  XIII) 


22 

Skull. 
(Chart  XVI) 


23 

Vertebral   col- 
umn. 
(Chart  X) 


INSPECTION 

Methods  of  Testing 

The  expression  of  the  patient's  face  indicates,  in  most  cases,  the  degree  of  his 
intelligence  and  his  emotional  state  (sad  or  gay  or  anxious),  and  also  may 
suggest  the  presence  of  certain  diseases  and  conditions;  such  as  myxedema 
and  cretinism  (( 116314).  acromegaly  (1183),  scleroderma  (1165),  exophthalmic 
goitre  (1193),  paralysis  agitans  (677),  myasthenia  (554),  nasal  obstruction, 
atheroma  of  temporal  arteries,  notched  teeth,  hazy  cornea,  the  saddle- 
back nose  of  syphilis,  etc.  His  general  appearance  and  behavior  often  indi- 
cate his  power  of  self  restraint  (inhibitory  power,  breeding),  or  the  existence 
of  hallucinations  (213)  of  sight,  hearing,  touch,  or  of  compulsory  acts  (218). 

The  walk  of  the  patient  may  suggest  the  presence  of  hemiplegia  (254),  p>ara- 
plegia  (257),  local  paralysis  (259),  ataxia  (motor  or  cerebellar)  (280-1),  spasm 
(242),  atony  (252),  paralysis  agitans  (677)  and  other  tremors  (250),  pseudo- 
hypertrophic paralysis  (500),  hysterical  paralysis  (527),  foot  drop,  (bilateral  in 
multiple  neuritis  and  lead  palsy,  unilateral  in  acute  anterior  poliomyelitis), 
weakness,  exhaustion,  etc. 

The  skull  should  be  observed  as  to  type  (brachy-  or  dolicho-cephalic,  round  or 
long  heads),  size  (microcephalic — small,  macrocephalic — large),  rickets  (box 
shaped),  general  or  local  hydrocephalus  (bulging — posterior  or  anterior), 
fontanelles  and  sutures,  asymmetry,  tumors,  etc- 

The  spinal  column  should  be  observed  as  to  curvature  (angular  or  lateral), scoliosis, 
kyphosis,  spina  bifida  (occultoj,  deformity  (dislocation).  Pott's  disease,  tumor, 
tenderness  (by  palpation),  etc. 


24 
Eye. 

(Charts  V, 
&  XIV) 


Note  the  existence  of  arcus  senilis,  the  condition  of  pupils  (unequal,  anisocoria 
(341),  miosis  (340),  mydriasis  (339),  and  irregularity), the  presence  of  keratitis 
or  iritis,  prominence  of  eyeballs,  nystagmus,  squint,  ptosis,  paralysis,  etc. 


25 

Pupillary   re- 
flex  to   light. 

(Charts   V   & 
XIV) 


26 

Hemiopic  re- 
flex. 

Charts  V  & 
XIV 

27 

Pupillary   re- 
flex to  ac- 
commo- 
dation. 

(Charts  V  & 
XIV) 


Note  whether  each  pupil,  the  other  eye  being  covered,  dilates  and  contracts  as 
the  eye  is  alternately  shaded  by  the  hand  and  exposed  to  light,  or  an  electric 
light  is  flashed  into  it ;  vision  being  constantly  fixed  upon  some  distant  object. 
When  a  pupil  contracts  to  light  (direct  reflex)  the  pupil  of  the  other  eye  also 
contracts  (consensual  reflex).  Naturally  a  pupillary  reflex  will  not  occur  when 
the 5ris  adherent  to  the  lensi  (posterior  synechia)  as  the  result  of  a  former  iritis, 
which  itself  is  often  due  to  syphilis  (in  which  disease  pupillary  reflexes  are  of 
much  importance)  or  to  rheumatism. 

Note  whether  the  pupil  contracts  as  light  is  flashed  on  each  half  of  the  retina 
alternately.  A  ray  of  light  collected  by  a  lens  should  be  used  in  this  test.  This 
reflex  is  difficult  to  obtain,  and  recent  researches  indicate  that  its  existence  is 
doubtful.  It  has  been  found,  however,  in  a  number  of  cases  and  verified  by  post- 
mortem findings  in  some  of  them. 

Note  whether  the  pupil  dilates  when  the  patient  looks  at  a  distant  object  and  con- 
tracts when  he  looks  at  one  so  near  his  face  as  to  require  convergence  of  the  eyes. 
This  test  can  be  made  on  a  blind  man  by  having  him  first  converge  his  eyes  and 
then  make  the  axis  of  his  eyes  parallel,  by  imagining  that  he  is  looking  at  a  near 
and  then  then  at  a  distant  object. 


46 


28 

Pupillary   re- 
flex to   pain. 

Charts,  V, 
XIV    (330) 

29 

Double  vision, 

diplopia. 
(Charts  VI  & 

XIV) 


30 

Secondary 
deviation  of 
the  sound 
eye. 

(Chart  XIV) 

31 

Nystagmus. 
(Charts  IV  & 
XII) 


32 

Tremor. 
(Charts   IV   & 
XII) 


33 

Convulsion 
and   spasm 

(Charts  IV 
&  XII) 

34 

Paralysis 
(motor). 

(Charts  IV, 
&  XIII) 


INSPECTION   (Continued) 

The  pupils  dilate  when  the  patient  suffers  acute  pain.  Therefore,  they  dilate  re- 
flexly  when  the  skin  of  the  face  is  sharply  pinched,  or  pricked  with  a  pm,  or 
irritated  by  electricity. 

Note  which  eye  deviates,  however  slightly,  from  the  direct  axis  of  vision  and  which 
eye  lags  more  or  less  on  movement  of  eyeballs  in  following  the  moving'  finger. 
Place  a  colored  glass  before  the  affected  eye,  move  a  bright  object  (candle) 
throughout  the  field  of  vision  and  have  the  patient  note  the  relative  position  of 
the  two  images.  The  colored  image  will  of  course  be  the  one  seen  by  the  affected 
eye. 

Hold  a  card  close  in  front  of  the  sound  eye.  Have  the  patient  look  at  an  object 
so  held  that  the  weakened  muscle  must  be  brought  into  action.  The  sound  eye 
covered  by  the  card  will  be  observed  to  move  too  far  and  when  the  card  is  re- 
moved the  sound  eye  will   quickly  move  back  into  proper  position. 

The  oscillation  of  the  eyeball  which  constitutes  nystagmus  is  often  plainly  to  be 
seen.  Extreme  deviation  of  the  eyeballs  in  one  direction  or  the  other  makes  it 
more  evident,  and  at  times  demonstrates  a  nystagmus  not  otherwise  apparent. 
If  present,  nystagmus  is  usually  recognized  while  making  the  two  tests  29  and  30. 
It  should  not  be  confounded  with  the  irregular  jerky  motion  of  a  weakened 
ocular  muscle  attempting  to  move  the  eyeball. 

Note  anv  tremor  of  lips,  or  other  parts  of  the  body.  Note  its  frequency, 
amplitude,  its  relation  to  voluntary  movements  and  whether  it  is  associated 
with  muscular  rigidity.  In  testing  for  tremor,  ask  patient  to  hold  arms  ex- 
tended before  him  or  over  his  head  with  fingers  spread  and  motionless ;  or 
observe  him  place  his  hand  in  his  trousers'  pocket. 

Note  any  convulsion  (269),  spasm  (245-6),  contracture  (263-4),  athetosis  (271), 
choreiform  movement  (272),  etc.,  which  may  be  present.     These  various  forms 
XI     of  spasm  are  often  difficult  to  recognize  and  differentiate  from  each  other. 

Note  any  obvious  paraJvsis.  such  as  ptosis.  Note  the  naso-labial  fold  and  the 
height  of  the  angle  of  the  mouth  on  each  side.  Wliile  under  close  mspection, 
patient  should  be  requested  to  execute  every  possible  motion:  i.e.,  wnnkle 
forehead  (look  upward,  or  open  eyelids  held  closed  by  obserx-er),  frown,  open 
and  shut  each  evelid,  move  eyeballs  up  and  down  and  to  either  side  (note 
whether  upper  eyelid  follows  eyeball  well  downwards),  whistle,  laugh,  distend 
cheeks,  raise  upper  lip  and  each  angle  of  mouth,  protrude  tongue  straight  and 
move  it  in  all  directions,  raise  uvula  in  phonation,  close  jaws  and  move  chin 
forwards  and  jaw  laterally,  contract  strongly  all  muscles  of  face  at  once  move 
head  backwards,  forwards  and  towards  each  shoulder  and  shake  it,  bend  body 
in  all  directions,  raise  arms  vertically,  raise  shoulder,  adduct  and  fbduct  arm 
flex  and  extend  elbow,  wrist  and  each  finger,  spread  fingers,  adduct,  abduct, 
flex  and  extend  thumb,  pronate  and  supinate  forearm  while  elbow  is  flexed 
stand  on  each  leg,  raise  body  on  tiptoes,  adduct  and  abduct  thigh,  flex  and 
extend  thigh,  leg,  foot  and  toes. 


X 


47 


35 

Paresis. 

(Charts  IV,  X 
&  XIII) 


INSPECTION  (Concluded) 

Make  strong  resistance  to  above  mentioned  movements  while  patient  is  executing 
them:  i.  e.,  pull  on  eyelids,  on  one  angle  of  mouth,  resist  movements  of  jaw,  or 
of  bending  head,  or  body,  or  of  flexing,  extending,  adducting  and  abducting 
joints,  compare  the  strength  of  the  paretic  muscle  with  that  of  a  similar  healthy 
one.  when  possible,  with  its  fellow  of  the  opposite  side  of  the  body.  For  future 
comparison,  etc.,  the  strength  of  the  paretic  muscle  can  be  registered  by  dyna- 
mometers, of  which  the  most  practical  is  the  one  for  the  hand  grasp.  Or  sufifi- 
dent  weights  may  be  placed  on  hand,  foot  or  head  to  overcome  the  attempted 
movement.  By  these  tests  the  degree  of  the  paresis  can  be  approximately 
measured. 

^       ,      .  Note  whether  patient  tires  easily  on  repeated  or  continuous  activity  of  any  set  of 

Myasthenia.  , 

(Chart  IV)  muscles. 

zf.  .      Note  whether  patient  can  alternately  extend  and  flex  joints  quickly  and  repeatedly. 

(Ch    t   1 V^  '^        '^^^'  especiaJly  rapid  alternate  supination  and  pronation. 


38 

Ankylosis. 


39 

Contracture. 
(Charts  IV  & 
XI) 

40 

Muscle  tone. 
(Charts  IV  & 
X) 


Note  whether  any  joint  is  rigid,  so  that  it  cannot  be  moved.  Ascertain  the  cause 
of  the  rigidity,  whether  bony  union,  contracted  muscle  or  contracted  scar  tissue 
(muscle,  ligament,  skin,  etc.). 

Note  whether  any  muscle  is  contractured  with  consequent  impaired  motility  of 
the  joint  and  whether  this  contracture  can  be  overcome  by  force,  with  or  with- 
out etherization  (active  contracture),  or  not  (passive  contracture). 

Note  whether  muscles  are  firm  or  flabby,  and  whether  or  not  resistance  is  offered 
to  rapid  motions  of  joints  while  the  patient  tries  to  avoid  voluntary 
resistance.  Normally  there  is  slight  resistance.  In  disease  the  resistance  may 
be  altogether  absent  (atonia),  or  weak  (hypotonia),  or  strong  (hypertonia). 


41  Note   whether   any    muscle    shows  atrophy  or  hypertrophy,  or  fibrillary  contrac- 

Irophic   lesions,     tions,  or  if  there  is  any  arrested  development  or  trophic  lesions  of  other  tissues 
(especially  ulcers,  herpes,  glossy  .skin,  abnormalities  of  nails,  etc.). 


(Chart  XVII) 


42 

Coordination 
(synergy). 

(Charts  IX  & 
XII) 


43 

Muscle  and 
joint   sense. 
Deep  sensi- 
bility (bath- 
yesthesia, 
kinesthe- 
sia). 

(Charts   VI    & 
XII) 


Note  w'ltther  complicated  movements  are  executed  in  an  orderly  manner  while 
the  patient's  eyes  are  closed.  Ask  patient  to  walk,  touch  point  of  nose  with 
finger  tip,  pick  up  objects,  write,  touch  knee  with  heel  of  other  foot,  hold  foot 
steady  in  one  position,  trace  a  circle  in  the  air  with  foot,  walk  backwards,  side- 
ways and  along  a  line,  stand  on  one  foot  alone  or  on  both  feet  close  together, 
either  side  by  side  or  one  in  front  of  the  other  (Romberg's  symptom),  stand  on 
tiptoes  or  on  heels,  stand  on  one  foot  and  trace  a  circle  on  the  floor  with  the  toe 
of  the  other  foot.     All  these  tests  should  be  made  both  with  eyes  open  and  shut. 

Note  whether  patient,  with  his  eyes  shut,  can  tell  whether  his  joints  are  flexed 
or  extended,  or  can  duplicate  with  one  extremity  the  position  in  which  his 
other  is  placed.  Note  whether  he  can  estimate  weights  correctly  or  can  grade 
by  weight  loaded  balls  correctly.  Note  whether  he  can  locate  his  extremities 
in  space.  To  test  this,  his  eyes  being  shut,  an  extremity  after  being  moved 
about  is  held  in  one  position  and  he  is  told  to  turn  his  head  and  eyeballs  so 
that  when  he  opens  his  eyes  he  shall  be  looking  directly  at  his  thumb  or  great 
toe.  When  he  opens  his  eyes  it  will  be  plain  to  see  whether  they  are  ditected 
right  or  not. 


48 


CHART  Ic 
Palpation  and  Percussion 

Comprising  Numbers  45  to  68 


49 


Methods  of  Examination  of  Patients  Suffering  from  Nervous  Diseases 


PALPATION  AND  PERCUSSION 

Methods  of  Testint. 

45  Note  the  color  of  the  skin,  the  pulsation  of  arteries  in  neck,  the  condition  of  the 

Circulation  and       jugular  veins  and  the  frequency  and  regularity  of  respiration,  especially  Cheyne- 
respira  on.  Stoke's  respiration  (425  ),  whether  respiration    he  costal  or  abnormal,  or  the  dia- 

phragm be  immobile,  unilaterally  or  bilaterallv. 


(Chart  XVII) 


46  Note  pulse  of  patient  as  to  frequency,  \olunie,  tension  (best  tested  by  tonometer 

i^r-u^      \'\ni\       °''  sphygmomanometer)  and  irregularity  in  rhvthm  and  force. 
( Chart   A.  V 1 1 ) 


47 
Difficulties   in 

sensory 

testing. 
(Chart  VI) 


The  result  of  all  sensory  tests  (and  the  same  is  true  in  regard  to  tests  for  many 
mental  symptoms)  depends  upon  the  patient's  truthfulness.  Deception  is 
always  possible  and  even  with  the  most  truthful  patients  the  tests  require 
much  time  and  the  results  are  often  contradictory,  especially  so,  in  e^■citable 
and  in  uneducated  patients,  who  cannot  iix  their  attention  continuously. 
Notliing  should  be  present  to  distract  the  patient's  attention  and  his  skin  should 
be  warm.  In  some  nervous  diseases  the  patient  has  occasional,  spontaneous 
sensations  which  interfere  with  the  tests.  Most  patients  under  the  education  of 
repeated  tests  become  more  acutely  sensitive.  On  the  other  hand,  tests  too  long 
continued  tire  the  patient  and  give  rise  to  contradictory  results.  It  is  to  be 
remembered  that  the  sensibility  of  the  skin  both  for  tactile  and  painful  impres- 
sions varies  greatly  in  diiiferent  parts  of  the  body  and  in  different  individuals. 


48 

Tactile  sen- 
sibility. 

(Charts  VI   & 
XIV) 


With  the  finger  tip  (or  with  a  smaller  and  lighter  object,  such  as  the  head  of  a 
]>in,  a  camel's  hair  bnish,  a  pledget  of  cotton,  a  hair,  etc.),  touch  the  patient's 
skin  lightly,  having  told  him  to  say  "yes"  every  time  he  feels  the  slightest 
touch.  Or  the  patient  may  describe  figures  (space  sense)  traced  on  his  skin  with 
ink  (to  prevent  dispute  or  doubt).  A  pledget  of  cotton  is  better  for  accurate 
testing  than  is  the  finger  tip  or  a  pin,  because  with  the  cotton  the  pressure 
sense  (49)  is  eliminated.  Of  course,  during  all  sensory  tests  the  patient's 
eyes  must  be  closed  or  covered.  In  some  cases  of  hysterical  anesthesia,  if 
the  patient  is  told  to  say  "no"  when  she  does  not  feel  the  touch,  she  will  say 
"no"  only  at  the  instant  she  is  actually  touched  within  the  anesthetic  ( ?) 
area;  showing  that  sensation  is  not  abolished,  although  it  may  well  be  abnormal 
(Janet's  test).  Tactile  sensibility,  or,  more  properly,  ".space  sense,"  or  "localiz- 
ing sense,"  (.^.3),  may  also  be  tested  with  the  esthe.siometer ;  a  pair  of  blunt 
dividers,  by  which  it  is  noted  how  far  the  points  may  be  separated  and  yet 
be  felt  as  one.  This  distance  varies  greatly  in  difl'crent  parts  of  the  body  (at 
the  point  of  tongue  it  is  one  m.  m.,  at  finger  tips  two  m.  m.,  along  back  and  on 
upper  part  of  arm  and  thigh  it  is  sixty-five  m.  m.  The  distance  is  smaller  trans- 
versely than  longitudinally  on  the  extremities.  Neither  this  compass  esthesi- 
ometer.  nor  Hering's  esthesiomcter  gives  more  valuable  results  than  the  pin- 
head  tests.  When  mapping  out  an  anesthetic  area  commence  in  the  anesthetic 
area  and  work  towards  the  normal  skin.  Do  the  reverse  in  mapping  out  hyperes- 
thesia; i.e.,  from  normal  skin  to  h\peresthetic  area.  The  electro-cutaneous 
test  can  be  more  accurately  measured,  but  is  of  little  practical  value. 


50 


PALPATION  AND  PERCUSSION  (Continued) 


49 

Pressure    sense. 
(Chart  VI) 

50 

Painful   sen- 
sibility. 

(Charts  VI  & 
XIV) 

51 
Retardation   of 

conduction. 
(Chart  VI) 

52 

Persistence  of 

sensation. 
(Chart  VI) 

53 

Localization. 
(Chart  VI) 

54 

Double   sensa- 
tion and 
polyesthesia. 

(Chart  VI) 

55 
Temperature 

sense. 
(Chart  VI) 

56 

Pallesthesia. 
(Chart  VI) 

57 
Cutaneous 

reflexes, 

(Chart   V) 


Note  whether  patient  can  estimate  correctly  the  amount  of  pressure  exercised  by 
the  finger  pressed  against  the  skin,  or  by  weights  laid  upon  it. 

Note  whether  patient  feels  pain  when  pinched,  or  when  skin  is  pricked  by  finger- 
nail, pin-point,  or  other  sharp  substance.  Many  instruments  have  been 
devised  for  measuring  more  or  less  accurately  the  intensity  of  the  painful 
impression.  -w 

Note  whether  the  painful  sensation  is  felt  immediately  upon,  or  some  seconds 
after,  the  painful  contact. 

Note  whether  the  painful  sensation  persists  a  longer  time,  after  the  painful  con- 
tact has  ceased,  than  is  normal. 

Note  whether  the  point  of  contact,  tactile  or  painful,  can  be  localized  correctly  by 
the  patient  either  by  description  or  by  pointing;  his  eyes,  of  course,  being  shut 
or  bandaged. 

Note  whether  a  single  or  painful  contact  causes  two  (double  sensation)  or  more, 
sensations  (polyesthesia). 


58 


Touch  the  sk-in  at  numerous  points  alternately  with  smatl  test  tubes,  one  filled 
with  hot,  the  other  with  cold,  water,  or  writh  hot  and  cold  bodies  (spoons)  of  the 
same  size  and  form.  Certain  points  of  the  skin  are  especially  sensitive  to  heat; 
others  to  cold.     It  is  well,  therefore,  to  test  for  heat  and  cold  separately. 

Note  whether  the  patient  feels  the  vibration  of  a  tuning  fork  (vibration  sense) 
pressed  so  firmly  on  the  skin  that  the  vibration  can  be  transmitted  through  the 
underlying  bone  (osseous  sense). 

Stroke  or  scratch,  as  softly  as  will  suffice,  with  finger  nail  or  head  or  point  of 
pin,  the  skin  of  the  sole  of  the  foot  (plantar  and  Babinski),  or  ai  buttock  (glu- 
teal), or  the  inner  side  of  thigh  (cremasteric),  or  the  side  of  abdomen  (umbil- 
ical), or  the  hypochondrium  (epigastric),  or  interscapular  region  (interscapu- 
lar),' or  stroke  firmly  along  the  postero-internal  border  of  the  tibia  (Oppen- 
heim's  reflex^  and  note  the  resulting  movement  of  the  great  toe.  The  muscle 
itself  must  be  felt  and  watched  in  cases  where  the  resulting  contraction  is  too 
slight  to  move  the  part. 


Cpharnygeal),  and  note  the  resulting  movement. 
Note  the  pallor  or  redness  of  the  skin,   also    rapid   changes  and  flushings  with  or 


Mucous  mem-    Touch  with  finger,  straw,  brush,  or  probe,  the   cornea   or   conjunctiva    (conjunc- 
brane  reflexes,     ^j     ^    ^j.  mucous  membrane  of  nose  (nasal),  or  palate  (uvular),  or  pharnyx 
(Chart  V) 

59 

Vaso-motor         ^,,^,.^  ,,.^    

,^^^T^^^vvIT^'' w'thout''irritatbn,  such  as  scratching  with  a  pin  or  finger-nail  (dermographia). 
(Chart  V  <x  A VII) 

60  With  leg  relaxed,  semi-flexed  and  well  supported,  strike  or  press  the  sole  of  the 

Ankle-clonus.  foot    quickly,    firmlv    and    continuously    upwards    and    note    whether  the  foot 

(Charts  V  &  oscillates  or  not.     This  clonus  occurs  at  times  spontaneously  when  the  toe  and 

^)  not  the  heel  rests  on  the  floor  ("spinal  epilepsy"). 


51 


PALPATION  AND  PERCUSSION  (Concluded) 


61 

Knee-jerk. 
( Charts  V  & 

X) 


While  patient  is  sitting  on  a  chair  with  legs  crossed,  or  better  on  a  table  with 
legs  hanging  free,  or  is  lying  in  bed  on  his  back  with  knees  flexed,  strike  the 
liganientum  patellae  a  sliarp  blow  with  the  finger,  edge  of  hand,  book  or  percus- 
sion hammer  and  note  whether  the  foot  flies  forward.  The  amplitude  of  the 
excursion  of  the  foot  is  not  alone  a  safe  guide  to  infer  increase  of  knee-jerk,  but 
rather  its  vigor,  its  quickness,  and  the  presence  of  two  or  three  additional 
oscillations  as  the  foot  falls  back  again.  Even  a  continuous  oscillation,  or 
clonus,  occurs  in  some  cases  (the  so-called  "spinal  epilepsy").  More  common 
than  this  clonus  is  a  simultaneous  contraction  of  the  adductors  of  the  other 
thigh  when  the  knee-jerk  is  exaggerated.  In  order  to  obtain  this  reflex  the  ob- 
server must  make  sure  that  the  muscles  of  the  legs  are  completely  relaxed.  The 
extensor  femoris  muscle  must  be  observed  and  felt  in  those  cases  where  the 
resulting  contraction  is  too  faint  to  move  the  leg.  Knee-clonus  may  be  obtained 
in  suitable  cases  by  grasping  the  patella  from  above  and  pulUng  it  sliarply 
downwards.  In  some  cases  of  disease  of  the  cerebellum,  in  testing  the  knee- 
jerk  the  leg  swings  backwards  and  forwards  like  a  pendulum;  the  normal  check 
restraint  being  absent  (Pendular  knee-jerk). 


62 

Achilles   reflex. 
(Charts  V  & 
X) 

63 

Dorsal  foot 

reflex. 
(Chart  V) 


Wliile  patient  is  knedling  in  a  chair  with  his  feet  projecting  free,  the  tendcK- 
Achillis  should  be  strongly  struck  with  a  percussion  hammer  and  the  movement 
of  plantar  flexion  noted.  Where  the  patient  cannot  kneel  the  leg  may  be  sup- 
ported in  any  position  which  relaxes  it  and  the  tendo-Achillis  struck. 

When  the  dorsum  of  the  foot  is  struck  sharply  over  the  4th  or  5th  metatarsal 
bone,  note  the  dorsal  (normal)  or  plantar  (pathological)  flexion  of  toes 
(Mendel-Bechterew's  reflex— 321,  457). 


64 

Elbow  and  wrist  '^^  ^^'^  being  relaxed,  well  supported  and  semi-flexed  at  elbow  the  tendons  at 

reflexes  elbow  or  wrist  are  sharply  struck. 

(Chart  V) 

65  The  patient's  chin  is  firmly  grasf)ed  with  finger  and  thumb  or  a  flat  stick  is  placed 
The  jaw  reflex,  jp  the  patient's  mouth  resting  on  his  lower  teeth,  tbe  mouth  being  half  open, 
( Chart  V  )  ^i^j  j,j^gj.|  jj.|g  ^jjj^^]^  Qj.  j-j^g  hand  hollding  chin  is  struck  sharply  downward  and  the 

closure  of  the  mouth  noted. 

66  With  thigh  flexed  at  hip  and  leg  flexed  at  knee,  the  patient  either  sitting)  or  lying, 
Kernig's  reflex.  the  leg  should  be  quickly  extended  at  knee  joint  and  a  strong-  resistance  to  such 
(Charts  V&  X.)        extension  noted,  if  present. 


67 

Mechanical 
irritability. 


Strike  the  nerve  or  muscle  sharply  with  the  finger  or  percussion  hammer  or  press 
the  nerve  trunk  or  its  tender  points. 


68 

Reinforce- 
ment. 


The  tendon,  and  to  some  extent  the  cutaneous,  reflexes  can  be  made  stronger 
and  can  be  often  made  to  appear  when  apparently  absent,  by  diverting  the 
patient's  attention  in  any  way,  usually  by  having  him  pull  strongly  on  his 
elapsed  hands,  his  eyes  being  turned  to  the  ceiling  or  to  a  picture  at  the  instant 
the  reflex  is  tested  (Jendrassik). 


52 


CHART  Id 

Electricity,  Lumbar  Puncture,  Brain  Puncture, 

Ophthalmoscopy,  Thermometry, 

Caloric  Reaction 

Comprising  Numbers  70  to  80 


53 


Methods  of  Examination  of  Patients  Suffering  from  Nervous  Diseases 


70 

Faradism. 
(Chart  VII) 


71 

Galvanism. 
(Chart  VII) 


ELECTRICITY  AND  LUMBAR  PUNCTURE 

Methods  of  Testing 

The  electrodes  should  be  kept  well  moistened  with  warm  salt  water  during  the 
testing.  The  larger  electrode  is  placed  on  sternum  or  back  of  neck  or  sacrum ; 
while  the  smaller  electrode,  provided  with  an  attachment  for  making  and 
breaking  (opening  and  closing)  the  current,  is  placed  over  the  motor  point 
of  nerve  or  muscle  (Chart  Vllb).  The  secondary  current  of  a  faradic  battery 
should  be  employed  and  the  current  should  be  gradually  increased  in  strength  by 
methods  which  vary  in  different  batteries,  until  the  faintest  distinct  contraction  of 
the  muscle  occurs  whenever  the  current  is  suddenly  closed,  the  negative  elec- 
trode being  over  the  motor  point.  The  test  should  be  repeated  several  times. 
As  the  skin  becomes  moister  a  less  strong  current  becomes  necessary.  It  is 
important  to  make  sure  of  the  exact  position  of  the  motor  point  in  each  case 
by  some  preliminary  tests  and  not  to  let  the  electrode  slip  away  from  this  point 
during  the  testing. 

With  the  electrodes  arranged  as  above,  first  the  negative,  later  the  positive, 
electrode  should  be  placed  over  the  motor  point  of  nerve  or  muscle  and  the 
strength  of  the  current  slowly  increased  by  means  of  the  rheostat  until  the 
faintest  distinct  contraction  of  the  muscle  occurs  whenever  the  current  is 
closed.  The  strength  of  the  current  causing  this  contraction,  with  each  elec- 
trode in  turn  over  the  motor  point,  should  quickly  be  read  from  the  galvano- 
meter, even  before  the  needle  has  quite  ceased  its  oscillations.  In  the  same 
way  read  from  the  galvanometer  the  strength  of  the  weakest  current  which 
will  cause  the  faintest  distinct  contraction,  when  each  electrode  in  turn  is  on 
the  motor  point  and  the  current  suddenly  opened. 


72 

Muscle  and  nerve 
(Chart  VII) 


In  all  cases  both  the  muscle  and  the  nerve  supplying  it  should  be  tested  both  bv 
faradism  and  galvanism. 


73  Note  the  character  of  the  muscular  contraction,  whether  quick  or  sluggish   (de- 

Lharacter  of  the  generative),  or  showing  any  peculiarity,  and  whether  it  is  unusually  persistent 
(myotonic),  or  whether  it  rapidly  grows  feebler  under  repeated  tests  (myas- 
thenic). 


contraction. 
(Chart  VII) 


74 
Lumbar 

puncture. 
(Charts  VII  & 

XIX 


The  patient's  body  should  be  bent  strongly  forwards.  Patient  should,  if  possible, 
sit,  but  may  be  lying  down.  The  skin  having  been  thoroughly  washed  with 
alcohol,  a  horizontal  line  should  be  drawn  from  the  posterior  spine  of  one  ilium  to 
that  of  the  other  and  a  sterilized  fine  needle  three  of  four  inches  long,  preferably 
of  platinum  and  with  ratlier  a  short  bevel,  should  be  inserted  between  the  laminae 
of  the  vertebrae  immediately  below  or  above  this  horizontal  line.  The  needle 
may  be  inserted  in  the  median  line  or  a  little  to  one  side  of  it  and  pushed  steadily 
forward  and  slightly  upward  until  it  enters  the  arachnoid  sac  when  usually  the 
cerebro-spinal  fluid  will  escape  in  drops.  If  the  needle  be  pushed  too  far  it 
can  be  felt  as  it  strikes  the  body  of  the  vertebra  and  it  should  then  be  with- 
drawn aljout  half  an  inch.  It  is  rarely  necessary  and  sometimes  dangerous  to 
attacli  a  syringe  and  aspirate  the  fluid.  If  the  needle  becomes  occluded  clear 
it  out  with  the  stylet.  It  is  better  not  to  withdraw  more  than  half  an  ounce 
of  the  fluid.  Note  the  rapidity  of  escape,  whether  by  drops  or  in  a  fine  stream 
(tension"),  its  appearance  (cloudy,  bloody,  purulent).  The  fluid  may  be  exainined 
chemically  (for  albumen,  sugar,  cholin,  etc.).  A  portion  of  the  fluid,  especially 
that  containing  the  fine  coagnlum  which  frequently  forms,  is  centrifuged,  the 
clear  fluid  is  carefullv  poured  off  and  the  bottom  of  the  tube  scraped  and 
aspirated  with  a  capillary  pipette,  the  content  of  which  is  spread  on  a  slide, 
fixed,  stained  and  examined  for  cells  (lymphocytes,  leucocytes,  bacteria,  etc.). 


54 


ELECTRICITY  AND  LUMBAR  PUNCTURE  (Concluded) 

The  cerebro-sfrinal  fluid  should  also  be  tested  for  an  increase  of  globulin,  indica- 
tive of  the  presence  of  a  s^'philitic  infection,  of  ancient  or  recent  date,  or  of  a 
meningitis,  according  to  the  method  suggested  by  Noguchi  (412).  After  lumbar 
puncture  patients  should  remain  quiet  in  bed  during  twenty-four  hours.  Even 
so,  they  are  apt  to  suffer  from  headache,  especially  if  much  fluid  has  been  with- 
drawn, or  withdrawn  too  rapidly.  Sometimes  the  nerve  trunks  of  the  cauda 
equina  are  injured,  causing  pain  in  the  legs,  but  such  pains  are  rarely  severe 
and  are  of  short  duration.  In  some  cases,  in  consequence  of  the  withdrawal  of 
the  cerebro-spinal  fluid,  the  medulla  and  cerebellum  have  been  drawn  down 
into  the  foramen  magnum  and  death  has  resulted  promptly.  Such  an  acci- 
dent is  only  possible  in  cases  of  cerebral  tumor  situated  in  the  posterior  fossa  of 
the  skull,  and  therefore  lumbar  puncture  should  not  be  performed  in  such  cases. 


BRAIN  PUNCTURE,  OPHTHALMOSCOPY,  LARYNGOSCOPY,  THERMOMETRY, 

AND  THE  CALORIC  REACTION 


75  _ 
Brain 
puncture. 


76 

Ophthalmoscopy 
(Chart  XIV) 

77 

Larvngoscopr. 
(Chart  XIII) 

78 

Thermom- 
etry. 


Caloric  reaction 
Baranv  test. 
(Chart  XII) 


80 
Cerebellar 

nystagmus. 
(Chart  XXI- 

causes). 


This  operation  consists  in  trephining  (with  avoidance  of  the  sinuses  and  large 
arteries)  a  small  button  from  the  scalp  and  bone,  inserting  a  very  thin  needle 
canula  and  aspirating  a  small  quantity  of  the  brain  substance,  or  tissue  of  a 
tumor,  or  fluid  from  a  cyst.  It  has  been  many  times  performed  and  the  results 
have  been  somewhat  encouraging,  but  it  is  an  operation  which  should  be  per- 
formed only  by  an  experienced  surgeon  or  neurologist  and  its  detailed  descrip- 
tion is  hardly  in  place  here. 

ExaiTiine  the  eyes  for  choked  disc  or  optic  neuritis,  and  for  optic  atrophy,  reti- 
nitis, miliary  tubercles,  etc. 

Examine  the  larynx  for  evidence  of  paralysis  of  one  or  more  or  of  all  its  muscles. 

ft  is  often  necessary  to  ascertain  the  temperature  of  the  patient.  The  thermom- 
eter should  be  well  washed  in  cool  water  both  before  and  after  taking  the  tem- 
perature. In  taking  the  temperature  in  the  mouth,  the  bulb  of  the  thermometer 
should  be  placed  well  under  the  tongue  and  it  should  be  noticed  that  the  lips 
are  held  tightly  closed  during  the  two  minutes  that  the  thermometer  is  left 
in  the  mouth.  In  taking  the  temperature  in  the  axilla,  the  axilla  should  first 
be  wiped  dry  from  sweat  and  care  should  be  taken  that  the  thermometer  be 
surrounded  by  skin  and  not  at  all  by  clothes ;  the  patient  should  be  rolled  over 
on  his  side  in  order  to  press  arm  firmly  against  chest  and  the  thermometer 
should  be  left  in  position  eight  minutes.  In  taking  the  temperature  in  the 
rectum,  a  little  vaseline  or  soap-suds  should  be  put  on  the  bulb  before  inserting 
it  into  the  rectum,  where  it  should  remain  two  minutes.  Instruments  have 
been  invented  for  taking  the  surface  temperature  of  the  skin  of  any  part  of 
the  body,  but  they  have  not  proved  to  be  of  much  practical  value. 

When  one  ear  of  a  normal  person,  with  head  held  upright,  is  syringed  out  with 
cool  water  there  results  a  horizontal  and  rotary  nystagmus  towards  the  other 
ear ;  when  water  warmer  than  the  body  is  used,  the  nystagmus  turns  towards 
the  syringed  ear.  This  reaction  does  not  occur  in  cases  of  destruction  of  laby- 
rinth, or  of  paralysis  of  the  vestibular  nerve  (403,  note). 

In  lesions  of  the  right  cerebellar  hemisphere,  nystagmus  to  the  right  may  only  be 
seen,  or  may  be  made  more  marked,  when  the  patient  lies  on  the  left  side  and 
vice-versa. 


55 


CHART  II 

Analysis  of  the  Etiological  Factors 
of  the  Case 

Comprising  Numbers  81  to  194 


S7. 


Analysis  of  the  Etiological  Factors  of  the  Case 


List  of  nervous  and  allied  diseases  likely  to  occur    as 
obtained  from  the  history  of  the  case. 


the    result   of    the    etiological  factors 


Bl  Heredity, 
including  eon- 
sanguineous 
marriages  in 
neuropathic 
families 
(Predisposing 
cause). 


84  Inherited 
Diseases 


Organic 
Diseases 


85  Inhexited 
Tendencies 


Neuroses 


Infancy  and 
Childhood 


82    Personal 
Factors 
(Predis- 
posing 

causes). 


86  Age 


^  101  Idiocy  and  Imbecility 

102  Spina  Bifida  and  Meningocele 

103  Hereditary  (Huutington'sj   Chorea 

104  Hereditary   (Friedreich's)   Ataxia 
-i  105  Myatonia  Congenita 

106  Myotonia  Congenita    (Thomsen''s   Disease) 

107  Muscular  Dystrophies 

108  Syphilis  of  the  Nervous  System 

109  Dwarfs  and  Giants 

[110  Insanity 

I  111   Epilepsy 

I  112  Hysteria 

^  113  Chorea 

I  114  Neurasthenia 

I  115  Neuralgia  and  Migraine 

[ll6  Drunkenness    (Alcoholism) 

[117  Cerebral  Palsy  of  Childhood 

118  Acute  Anterior  Poliomyelitis 
■  119  Meningitis    (tuberculous,    etc.) 
!  120  Hydrocephalus 

121  Tetany 
1  And  all  the  inherited  diseases  except  103 


Childhood 
Youth 


and 


i'122 
123 
124 
125 
126 


Caries  of   Spine  and  Compression   .Myelitis 
Meningitis   (tuberculous,  etc.) 
Hereditary  Ataxia 
Glioma 


Chorea 

127  Epilepsy 

128  Muscular 

129  Hysteria 

130  Insanity 


Dystrophies 


Adult 


-All  other    forms   of    Nervous   Diseases  and 
many  of  those  above  given 


87  Sex 


More  common     i^^^  ^y'^^f  ^    ■    r  : 
i  132  Exophthalmic  Goitre 

m  women  i  -, ,   xt 

^133  Neuroses 


88  Race 


89  Dwelling 
Place, 
Habitation 


More  common 
in  men 

I  Jewish  &  Latin 
^  Anglo-Saxon 

I  Tropica] 

L  Dampness 


^134  Locomotor  Ataxia   (Tabes) 

135  Paresis 

136  Injuries 

137  Organic  Diseases 

138  Neuroses 

139  Organic  Diseases 

[140  Reri-Beri 

i  141   Leprous  Neuritis 


90  Occupa- 
tion 


f 


Overstrain 


t  Poisons 


58 


\\M  Sleeping   Sickness 

143  Neuritis 

144  Occupation   Neuroses 

145  Neuritis 


83  Etiological 
Factors 
(Inciting 
causes) 


91    Trauma- 
tism 


92  Poisons 
Toxic 


93  Infec- 
tions 


94  Syphilis 


Physical 


Psychical, 

Acute-  and 
Chronic 


f 


Metallic 


Alcoholic 

Tobacco,  Tea 

or  Coffee 

Narcotic 


Germs  and 

Toxines 


(  Tertiary 
Syphilis 


95  Exhaus- 
tion 


96  Extension 
of  Inflam- 
mation 


Post- Syphilitic 
Infections 

From   Illness, 

Overstrain, 

Worry 
From  Venery 

and 

Masturbation 


1^146  Wounds  and  Injuries 

I  147  Hemorrhage  in   Brain,   Cord  or   Membrane 

I  148  Meningitis 

I  149  Myelitis 

I  150  Disseminated  Sclerosis 

151  Neuritis 
i  152  Tumors 
[^153  Abscess 

154  Hysteria 
.155  Insanity 

156  Neurasthenia 
tl57  Traumatic  Neuroses 

[158  Arsenical  Neuritis 

I  159  Lead  Palsy,  Colic,  etc. 

1^160  Mercurial  Tremor 

\  161   Multiple  Neuritis 
(  162  Neurasthenia 

163  Tremor 

164  Neurasthenia 

165  Drug  Poisoning;  Acute  or  Chronic 

f  166  Neuritis 

167  Meningitis 

168  Myelitis 

I  169  Acute  Anterior  Poliomyelitis 
i  170  Landry's  Paralysis 

171  Neuralgia 

172  Tetanus 

173  Hydrophobia 

174  Abscess 

[175  Gumma 

I  176  Meningitis  Gummosa 
1  177  Neuritis   Syphilitica 
1,178  Endarteritis  Syphilitica 

179  Locomotor  Ataxia 

180  General  Paresis  '■' 


181  Neurasthenia 

182  Hysteria 

183  Neurasthenia 


I  184  Cerebral   or  Spinal   Abscess 
185  Sinus  Thrombosis 
Caries   of    Skull  ,  186  Meningitis 
or  Vertebra*   I  187  Myelitis 
l188  Neuritis 


97  Arterial  Disease 

98  Metastasis  from  Other 
Organs 


[189  Apoplexy  ("cerebral,  spinal  or  meningeal) 
-'  189a  Thrombosis,  Cerel)ral  and  Spinal 
1^190  Intermittent  Claudication 


n91   Tumors 


99  Disease 
of  Other 
Organs 


192  Tuberculous  and   Suppurative  Meningitis 

193  Uremia 


f  Bright's  Disea^'F 

Diabetes 
'^      Mellitus  194  Diabetic  Coma  and  Neuritis 

1    100  Colfl  is  a  doubtful  direct,  but  probably  an  aiixiliary,  etiological  factor. 

59 


CH|ART  III 
Disturbances  of  Mental  Activity 


Analysis  of  the  Symptoms  of  the  Case  (Semeiology) 

Definition,  Significance  and  Reladonship  of  the  Symptoms  of  Disease. 


200 

Disturbances 
of  Mental 
Activity. 
(More   fully 
described 
and  discussed 
in  the  intro- 
duction 
Page  5). 


201 

CONSCIOUSNESS 

The  appreciation  of  one's  existence  and 
individuality  as  separate  from  the  rest 
of  the  universe  (Subject  conscious- 
ness). The  content  of  consciousness 
is  the  sum  of  the  present  perceptions 
of  the  various  sensations  (Object  con- 
sciousness), together  with  the  mem- 
ories of  past  perceptions  and  judg- 
ments (Experience)   (Chart  XVI). 

202 

INTELLIGENCE 

The  {xjwer  of  ascertaining  facts  and  rea- 
soning upon  them.  The  power  of  dis- 
covering the  relation  of  things  and  of 
acquiring  knowledge   (Chart  XVI). 

-I  203 

MEMORY 
I  The  power  of  retaining  in  the  mind  and' 
I  of  recalling  at  will  perceptions  and 
ideas  formerly  received.  The  more 
striking  the  perception  and  the  more 
frequently  it  is  repeated  or  recalled, 
the  better  becomes  its  memory  (Chart 
XIII). 

204 

EMOTIONS 

An  emotion  is  a  state  of  consciousness 
accompanied  by  a  feeling  of  pain, 
pleasure,  fear,  anger,  wonder,  scorn, 
etc.  In  health  a  person's  emotion  is 
usually  in  harmony  with  his  environ- 
ment, but  in  disease  it  may  be  quite  in- 
dependent of  the  environment  (Chart 

I    x\a). 


In  disease,  consciousness  and  intelligence 
may  be  either  diminished  or  perverted 
as  is  set  forth  in  Chart  III  a. 

Neither  intelligence  nor  consciousness  is 
exaggerated  or  increased  in  disease, 
although  the  latter  may  be  apparently 
so  (Self-consciousness).  In  such 
cases,  however,  there  is  a  concentra- 
tion or  limitation  of  consciousness 
rather  than  an  increase  of  it;  an 
exaltation  of  the  subject,  with  a  lower- 
ing of  the  object,  consciousness. 


In  disease,  memory  may  be  diminished 
in  whole  or  in  part,  and  the  emotions 
may  be  either  diminished  or  exagger- 
ated as  is  set  forth  in  Chart  b. 

Memory  is  never  increased  in  disease, 
although  certain  memories  may  be 
accentuated  and  others  lost;  even  all 
may  be  lost. 


61 


CHART  Ilia 
Disorders  of  Consciousness  and  Intelligence 

Comprising  Numbers  201  and  202,  and  205  and  218 


#3 


Analysis  of  the  Symptoms  of  the  Case  (Semeiology) 


Diagnostic 
Symptoms 


CONSCIOUSNESS 


Definition 


201 
C 
0 
N 
S 
C 
I 
0 
U 
S 
N 
E 
S 
S 


D 
I 
M 
I 
N 
I 
S 
H 
E 
D 


'  205  The  patient  lies  in  a  profound  stupor  from 

Coma  which  he  cannot  be  aroused  by  irritation 

of  any  sensory  organ  (eye,  ear,  skin, 
mucous  membrane,  etc.)-  No  voluntary 
acts  are  performed  and  the  reflexes  are 
abolished  or  diminished,  except  the  circu- 
latory and  respiratory,  which  are  often, 
but  not  always,  deranged.  Patient  is  un- 
able to  swallow.  Lips  and  cheeks  puff 
out  during  expiration. 

206  The  patient  is  apparently  in  a  coma  but  by 

-!  Semi-coma      strong  sensory  irritation  can  be  aroused 
or  to   some  manifestation  of   consciousness. 

Stupor  No  voluntary  acts  are  performed,  but  the 
reflexes  are  usually  present.  Patient  can 
swallow.  Patient  may  lie  apparently 
awake,  but  really  imconscious,  with 
a  low  muttering  delirium   (Coma  vigil). 

The  patient  lies  in  a  deep  sleep  or  moves 
about  automatically.  Can  be  rather  easily 
aroused,  but  does  not  fully  appreciate  his 
surroundings.  Can  speak  more  or  less 
intelligently. 


207 

Dazed,  Be- 
wildered, 
Somno- 
lence or 
Sopor 


SlGNIFICANCl 

These  three  conditions  are 
not  always  sharply  dif- 
ferentiated, but  may 
merge  into  each  other. 
They  are  due  to  loss  or 
diminution  of  brain 
function  in  consequence 
of  pressure  upon  the 
brain  or  of  circulatory 
disturbances  in  it,  or  of 
poisons,  etc.  They  occur 
in  traumatism,  and  in 
many  organic  diseases 
of  the  brain  and  its 
membranes  and  especi- 
ally of  its  blood  vessels; 
also  when  toxic  sub- 
stances (morphia,  etc.) 
or  toxins  (fever)  are  in 
the  blood;  also  in 
Bright's  disease  and  dia- 
betes mejllitus.  Rarely 
the  condition  is  func- 
tional. 


P 
E 
R 
V 
E 
R 
T 
E 
D 


r208 
Erroneous 
personal- 
ity 

209 
Double 
personal- 

.'^    . 
Dissocia- 
tion of 
personal 
ity 


210 

Auto- 
matism 

Somnam- 
bulism 


A  mental  condition  in  which  a  person  imagines  himself 
to  be  different  from  what  he  really  is;  sometimes  an 
animal,  sometimes  a  famous  character  in  history, 
sometimes  God,  etc. 

At  intervals  the  patient  is  in  a  sort  of  somnambulistic 
--'rite  and  presents  an  abnormal  consciousness  and 
!•  rsonality.  His  memory  at  times  is  .said  to  change 
wih  his  personality,  in  which  case  he  remembers  only 
o,  urrences  in  former  similar  conditions  and  not 
those  of  his  normal  state,  and  vice  versa.  This  lat- 
ter is  a  very  rare  and  doubtful  condition  and  offers 
much  opportunity  for  deception,  and  in  .some  cases 
of  hysteria  may  well  be  suggested  by  the  examining 
]>hysician. 


Occurs  in  insanity 
( f  unctionail ) . 


Occurs  in  hysteria 
and  epilepsy 
(functional). 


A  person  performs  complicated  and 
apparently  intelligent  acts,  while 
suffering  from  loss,  or  great  im- 
pairment, of  consciousness,  and 
retains  little  or  no  memorj'  of  the 
acts  done. 


Brain  is  probably  anemic  or  ex- 
hausted, or  the  patient  is  under  the 
influence  of  a  great  emotion 
(fright). 

Occurs  in  epilepsy,  insanity, 
hypnotism,  and  rarely  in  hysteria 
(functional);  not  uncommon  in 
childhood  during  sleep. 


64 


Diagnostic 

Symptoms 


202 

I 
N 
T 
E 
L 
L 
I 
G 
E 
N 
C 
E 


I 

M 
I 

I 

S 
H 
E 
D 


I  211 
Amentia 


212 
Dementia 

I 

^213 
Hallucina- 
tions 


214 
Illusions 


215 
Delusions 


INTELLIGENCE 

Definition 

Absence  or  defect  of  intelligence, 
winch  is  congenital  or  is  acquired 
in  infancy  before  the  intelligence 
has  developed. 

Absence  or  defect  of  intelligence, 
which  is  acquired  in  later  life  in 
a  person  previously  intelligent. 


Significance 

Due  to  a  malformed  or  diseased 
brain.  Occurs  in  idiots,  imbeciles 
and  feeble-minded  persons. 

Due  to  atrophy  or  functional  fail- 
ure or  diminution  of  blood  sup- 
ply of  cerebral  cortex.  Occurs 
in  insanity  and  is  often  its 
terminal  stage. 


216 

Hypochon- 
driasis 

217 
Delirium 


218 

Compulsory 
ideas  and 
actions 
(275) 


I. 


Vivid  perceptions  of  sensations  (visual,  auditory,  ol- 
factory, tactile,  painful,  etc.)  not  directly  depen- 
dent upon  any  external  corresponding  reality;  a 
sensation  without  an  external  object.  They  may 
rarely  occur  in  normal  individuals  and  then  may  be 
recognized  or  proved  to  be  false,  but  they  are  usually 
regarded  as  real  and  are  then  associated  with  defect- 
ive judgment  and  mental  impairment,  and  therefore 
cannot  be  corrected. 

Erroneous  perceptions.  A  false  interpretation  of  an 
actual  sensation,  which  is  really  of  a  dififerent  nature 
from  that  which  the  patient  believes  it  to  be.  Fre- 
quently occurs  in  rational  persons,  especially  in  those 
with  defective  terminal  sensory  organs.  In  such 
cases  easily  corrected. 

Erroneous  judgments  (often,  but  not  always,  depen- 
dent upon  hallucinations)  which  can  be  corrected 
neither  by  reason,  nor  by  the  evidence  of  the  senses 
and  which  are  not  in  accord  with  universal  human 
experience,  and  are  the  consequence  of  mental  en- 
feeblement.  Delusions  are  systematized  or  un- 
systematized according  as  they  are  supported  or 
explained  by  more  or  less  coherent  reasoning,  or 
not.  The  systematized  delusions  are  of  much  more 
serious  prognosis. 

Delusions  of  imaginary  symptoms  and  illness  formed 
on  an  insufficient  basis  of  abnormal  sensations,  which 
cannot  be  corrected  and  are  associated  with  much 
mental  depression. 

Irrational  talk,  or  acts,  or  both  in  persons  with  di- 
minished consciousness.  Probably  due  in  most  cases 
to  hallucinations,  illusions  and  mental  confusion ; 
consequently  its  irrationality  may  be  in  part  only 
apparent.     Often  occurs  in  fevers. 

Certain  thoughts  or  questions  or  doubts,  which  are  for- 
ever in  the  patient's  mind  and  cannot  be  removed. 
They  may  be  of  any  nature.  Patients  are  irresistibly 
compelled  by  an  unknown  force  to  do  certain  acts  or 
to  say  certain  words,  usually  quite  trivial.  Patients 
recognize  the  abnormal  character  of  these  ideas  and 
acts  and  are  made  very  unhappy  by  them,  but  are 
quite  unable  to  prevent  them. 


Due  to  disease 
of  the  cerebral 
cortex,  whether 
functional,  cir- 
culatoTy,  toxic 
or  organic 
Usually  symp- 
toms of  insan- 
ity, or  of  ex- 
t  r  e  m  e  degree 
o  f  neurasthe- 
nia, are  also 
present.  In  in- 
sanity these 
perversions  of 
intelligence  can- 
not be  correct- 
ed by  reason 
and  demonstra- 
tion, and  in  neu- 
rasthenia are 
only  rarely  and 
imperfectly  so 
corrected. 


Methods  for  the  detection  of  disorders  of  consciousness  and  intelligence  are  described  in 
Chart  la. 

For  further  discussion  of  these  symptoms  and  the  diseases  in  which  they  occur  see  Chart 
XVI. 

f5 


CHART  Illb 
Disorders  of  Memory  and  Emotions 

Comprising  Numbers  203  and  204  and  220  to  237 


67 


203 
M 

E 

M 
0 
R 
Y 

D 
I 

M 
I 

N 
I 
S 
H 
E 
D 


Analysis  of  the  Symptoms  of  the  Case  (Semeiology) 

MEMORY 

Definition  Significance 
Inability  to  recall  former  perceptions  and  Functional  or  organic  dis- 
ideas.  Loss  of  memory  in  general.  May  ease  of  the  cerebral  cor- 
be  more  or  less  extensive.  May  affect  tex,  often  anemia,  some- 
memories  of  the  immediate,  or  of  the  re-  times  the  result  of  fright, 
mote,  past. 


Diagnostic 
Symptoms 
220 
Amnesia 


221  Inability,    more    or   less   complete,    to    rec- 
Agnosia  ognize   objects    and    acts,    their  uses  and 

meanings,  which  were  formerly  well 
known ;  the  sensory  nerves  and  end-or- 
gans and  projection  fibers  being  normal. 
Such  patients  perform  idiotic  and  insane 
acts  and  put  formerly  well  known  objects 
to  absurd  uses  (urinate  in  water  pitcher, 
etc.).  It  may  be  regarded  as  a  local 
amnesia.  Among  the  various  forms  of 
agnosia  are:  Asterognosis  (230),  Alexia 
(229),  Agraphia  (228)  and  the  different 
forms  of  Sensory  Aphasia  (223-6). 

222  Inability  to  express  by  words  some  idea  in 
Motor    _  the  patient's  mind,  although  there  is  no 

aphasia  paralysis    of    the    vocal    organs  and  the 

(aphemia).       patient  can   usually   express  the  idea  by 

gesture.     A  loss  of  memory  of   how  to 

speak   (innervation  memories),  especially 

names.     A  limitation  of  the  vocabulary. 

223  Inability  to  understand  (although  not  deaf) 
Sensory  or  spoken  words  formerly  intelligible.  Loss 

Auditory  of    memory    of    words    formerly    heard, 

aphasia  Hence  inability  to  recognize  them  when 

(word  spoken   (233). 
deafness) 

224  Inability  to  name  objects,  which  the  patient 
Optic  sees  clearly,  although  he  can  name  them 

aphasia  after  feeling  them.  Loss  of  visual  memo- 

ries  (232). 

225  .    .        . 
Mixed               Amixttire  of  the  three  forms  of  aphasia  just 

aphasia  described. 

226  The  use  of  a  wrong  word,  or  the  omission 
Paraphasia  of    a   word,    or    the  placing  of  the  right 

(Jargon  word    in    the    wrong    place,  in  speaking, 

speech)  with      consequent      incoherent      speech. 

Jargon   speech  is  an  extreme  degree  of 

ithis. 

227  The  use  of  a  wrong  word, or  the  omission  of 
Paragraphia         a  word,  or  the  placing  of  the  right  word  in 

the  wrong  place,  in  writing. 

228  Inability  to  express  in  writing  the  idea  in 
Agraphia  the  patient's  mind,  although  he  formerly 

could  do  so  and  his  right  arm  and  hand 
are  not  paralysed. 

229  Inability  to  read  words  patient  could   for- 
Alexia  .  merly  read,  although  he  sees  them  clearly 

(Word  and  there  is  no  paralysis  of  his  vocal  or- 

blindness)         gans. 

68 


Lesion  of  a  cortical  sen- 
sory center,  or  of  the 
association  fibers  con- 
nected with  that  center. 


Lesion  in  or  near  base  of 
left  inferior  frontal  con- 
volution and  anterior 
portion  of  left  island 
of  Reil  in  right-handed 
persons,  and  of  the  right 
side  in  left-handed  per- 
sons. 

Lesion  in  or  near  posterior 
part  of  left  superior  tem- 
poral convolution  and 
posterior  portion  of  left 
island  of  Reil  in  right 
handed  persons. 

Lesion  of  left  occipital  lobe 
or  of  association  fibers 
from  this  lobe  in  right 
handed  persons. 

Any  one  or  a  combination 
of  the  above  lesions,  or  a 
lesion  of  the  island  of 
Reil,  or  of  external 
capsule  in  right-handed 
persons,  in  whom  the 
above  lesions  are  always 
in  the  left  cerebral 
hemisphere,  or.  in  slight 
degree,  may  result  from 
carelessness,  or  alcohol- 
ism, or  a  mild  dementia. 

Lesion  in  the  base  of  the 
middle  left  frontal  con- 
volution, cortical  or  sub- 
cortical. 

Sub-cortical  lesion  beneath 
left  angular  convolution 
in   right-handed  persons. 


Diagnostic 
Symptoms 

230 

Aster  e- 
ognosis 

231 

Apraxia 
(282) 


232 

Psychic 
blindness 

233 

Psychic 
deafness 


Definition 

Inability  to  recognize  objects  by  the  sense 
of  touch,  although  there  is  no  anesthesia 
present  in  sufficient  degree  to  prevent  it. 


InabiHty  to  execute  a  desired  act.  Loss  of 
skill  in  executing  acts,  although  there  is 
no  motor  paralysis  present.  Loss  of  in- 
nervation memories  necessary  to  perform 
these  acts. 

Inability  to  recognize  well  known  objects 
or  to  comprehend  familiar  things  by  sight, 
although  the  patient  is  not  blind.  Loss  of 
visual  memories,  optic  aphasia  (224). 

Inability  to  recognize  and  comprehend  well 
known  words  and  sounds,  although  the 
patient  is  not  deaf.  Loss  of  auditory 
memories.  Includes  sensory  aphasia 
(223). 


Significance 

Lesion  in  or  near  cortex, 
or  sub-cortex,  of  contra- 
lateral posterior  central 
convolution. 

Cortical,  or  sub-cortical, 
lesion  of  motor  area  of 
contralateral  hemisphere. 


Cortical,  or  sub-cortical, 
lesion  of  left  occipital 
lobe,  except  in  region  of 
calcarine  fissure. 

Cortical,  or  sub-cortical, 
lesion  of  left  superior 
tempwral  convolution  in 
right-handed  persons. 


204 
E 
M 
0 
T 
I 
0 
N 
S 


234 

Sadness 
(Melan- 
cholia) 


235 
Fear 

(Phobias) 


D 

I 

M 

I 

N 

I 

S    237 

H     Apathy 

E 

D 


236 
Joy 

(Mania) 


EMOTIONS 

Without  adequate  cause  the  patient  is  de- 
pressed and  unhappy.  There  is  a  great 
repression  of  mental  and  physical  activity 
usually.  He  can  be  influenced  little,  if  at 
all,  by  reason ;  difficult  to  get  his  attention. 

Without  adequate  cause  the  patient  is  in 
constant  fear  of  an  impending  calamity, 
or  has  an  unformulated  fear.  He  has 
an  unreasonable  fear  of  the  danger  of 
contamination  from  filth,  germs,  etc., 
(mysophobia).  He  dreads  to  cross  an 
open  space  (agoraphobia),  or  to  enter  a 
small  room  or  confined  space  (claustro- 
phobia), or  fears  a  storm  (astropholiia  ), 
or  syphilis  (syphilophobia),  or  ill-timed 
urination  (urophobia),  or  everything 
(pantophobia),  etc.  Can  be  influenced 
httle,  if  at  all,  by  reason.  Frequently 
has  a  more  or  less  unconscious  sexual 
basis. 

Without  adequate  cause  the  patient  is  exhil- 
arated. There  is  great  exuberance  of  men- 
tal and  physical  activity.  Careless  and 
destructive.  Can  be  influenced  little,  if  at 
all,  by  reason.  Difficult  to  get  his  at- 
tention. 

Without  adequate  cause  patient  is  in  a  dull, 
stuporous  condition.  No  expression  of 
physical  or  mental  activity.  An  auto- 
maton, submitting  passively  to  whatever 
is  done  to  him. 


Functional  or  circulatory 
disturbance  of  cerebral 
cortex,  especially  cere- 
bral exhaustion.  Occurs 
in  neurasthenia  and 
especially  in  insanity. 

Fears  and  apprehension 
seem  to  be  the  basic 
symptoms  of  many 
forms  of  incipient  in- 
sanity  (Mosher). 


Methods  for  the  detection  of  disorders  of  memory   and   emotion   are  described  in  Chart  la. 
For  further  discussion  of  these  symptoms  and  of  the  diseases  in  which  they  occur  see  Oiarts 
XIII  and  XVI. 


69 


CHART  IV 
Disorders  of  Voluntary  Motion 

ANALYSIS  OF  THE  SYMPTOMS  OF  THE  CASE  (SEMEIOLOGY) 
Definition,   Significance  and  Relationship  of  the  Symptoms  of  Disease. 


240 

DISORDERS  OF  VOL- 
UNTARY MOTION 

The  power  of  executing 
movements  by  an  effort 
of  will  is  acquired  in 
early  life.  The  process 
is  quite  obscure,  but 
seems  to  depend  upon 
the  existence  of  innerva- 
tion memories  of  past 
acts,  primarily  reflex. 
Voluntary  motion  de- 
pends ufKm  the  integrity 
of  the  central  motor  neu- 
rons (461 )  and  of  the 
peripheral  motor  neuro-i<: 
(462).  In  disease  the 
power  of  voluntary  mo- 
tion may  be  diminished, 
exaggerated  or  per- 
verted. 

MUSCULAR  TONICITY 

Closely  connected  with  the 
power  of  voluntary  and. 
involuntary  action  is  the 
fact  that  the  muscles  of 
a  normal  person  are  in 
a  condition  of  constant, 
slight,  but  varying,  con- 
traction. This  is  called 
mu.scular  tonicity  or 
tone.  It  is  really  a  re- 
flex act  caused  and  main- 
tained by  many  slight  ir- 
ritations, and  can  be 
abolished  by  cutting  the 
posterior  nerve  roots. 
Muscular  tonicity  is  in- 
creased (hypertonia)  in 
destructive  lesions  of  the 
central  motor  neurons 
and  in  some  functional 
disorders.  It  is  di- 
minished (hypotonia), 
or  abolished  (atonia). 
in  destructive  lesions  of 
the  peripheral  motor  or 
sensory  neurons,  in 
lesions  of  the  cerebellum. 
in  sleep  and  in  narcosis. 


241 

DIMINUTION 
also  called 
AKINESIS  and 
HYPOKINESIS 


243 
PERVERSION 

also  called 

PARAKINESIS 


242 
EXAGGERATION 

also  called 

HYPERKINESIS 


71 


f  244 

PARALYSIS 

A  condition  in  which  the 
muscles  cannot  be  con- 
tracted by  the  strongest 
effort  of  the  will.  As 
commonly  used  the  term 
includes : 

PARESIS 

A  condition  in  wliich  the 
muscles  can  be  contract- 
ed only  feebly  by  the 
strongest  effort  of  the 
will. 

f  245 

TONIC  SPASM 

A  continuous,  involuntary, 
muscular  contraction  of 
longer  or  shorter  dura- 
tion (572). 

246 

CLONIC  SPASM 

More  or  less  rhythmical 
alternations  of  involun- 
tary, coarse,  violent  mus- 
cular contractions  and 
relaxations.  Must  not 
be  confounded  with  a 
coarse  tremor  (571). 

247 

IRREGULAR  SPASM 

Tnvoluntarv  acts  of  various 
L      kinds  (293-4,  573-4). 

248 

ATAXIA 

Disorderly  movements  due 
to  loss  of  power  of  co- 
ordination (638).  Asy- 
nergia  (281-2).  Asso- 
ciated with  hypwtonia 
(252).  Dysmetria  (289.) 

249 

LOSS  OF  SKILL, 
APRAXIA 

Awkwardness. 

250 
^  TREMOR 

Involuntary  rhythmical  os- 
cillation of  some  part  of 
the  body  or  of  a  muscle. 
I  Less  pwwerful,  more 
rapid  and  more  rhyth- 
mical than  a  clonic 
I  spasm  but  similar  in 
appearance,  especially 
when  coarse.  Tremor 
may  be  slow  (3  to  6  per 
second)  or  rapid  (8  to 
12  per  second).  It  may 
^      be  coarse  or  fine  (639). 


'The  conditions 
under  which 
paralysis  or 
paresis  occurs 
are  set  forth 
in 
Chart  IV  a 


The  conditions 
under  'which 
the  various 
forms  of 
spasm  occur 
are  set  forth 
in 
Chart  IV  b 


The  condStians 
undeV  "which 
the  various 
forms  of  per- 
version o  f 
motion  occur 
are  set  forth 
in 
Chart  IV  c. 


CHART  IVa 
Motor  Paralysis 

Comprising  Numbers  244  and  251  to  260 


7A 


Analysis  of  the  Symptoms  of  the  Case  (Semeiology) 


244  PARALYSIS 


CHARACTER 

EXTENT 


p 

0 

A 

H 

R 

A 

A 

R 

L- 

A 

Y 

C 

S 

T 

I 

E 

S 

R 

Diagnostic 
Symptoms 

r  251 

Spastic,  or 
hyper- 
tonic, 
paralysis. 
(473). 

(Figs.  24-6) 


252 

Flaccid,   or 
hypo- 
tonic, or 
atonic,  or 
atrophic 
paralysis 
(472). 

(Figs.  24-6) 


253 

Myasthenic 
paralysis 
('554) 


MOTOR   PARALYSIS 


Definition 


A  paralysis  in  which  the  muscles  show  in- 
creased tone  and  offer  much  resistance  to 
passive  motion,  especially  rapid  motion. 
The  normal  excursion  of  the  joint  is  re- 
stricted. The  muscles  have  their  normal 
volume  and  under  the  microscope  their 
fibers  show  a  normal  appearance.  The 
electrical  reaction  of  muscle  and  nerve  is 
normal  (394).  The  tendon  reflexes  are 
increased. 


Significance 

Destructive  lesion  of  cen- 
tral motor  neurons(461). 
It  occurs  in  diseases  of 
the  brain  or  spinal  cord, 
or  may  be  functional. 
Rarely  a  reflex  spasm 
(268),  especially  pre- 
putial irritation  in 
children,  or  pain,  may 
simulate    this    condition. 


A  paralysis  in  which  the  muscles  have  lost 
their  tone  and  offer  little  or  no  resist- 
ance to  passive  motion,  even  when 
rapid.  The  joint  has  a  normal  or  even 
increased  excursion.  The  muscles  ex- 
hibit a  great  and  rapid  atrophy,  and 
under  th(  microscope  their  fibers  show 
a  loss  of  their  transverse  striation  and 
various  forms  of  degeneration  (fatty, 
hyaline,  etc.).  The  electrical  reaction 
of  degeneration  is  present  (397).  When 
muscles  are  completely  degenerated 
(402)  pa  sive  contractures  (263)  may 
occur,  in  which  stage  the  flaccidity 
and  free  ( xcursion  of  the  joint  are  lost. 
The  tendon  reflexes  are  abolished  or  di- 
minished. 


A  rapid  tiring  of  muscles  ujx)n  exercise.  A 
myasthenic  reaction  to  electricity  (399.) 
Muscles  show  small  foci  of  small  round 
cells. 


Destructive  lesion  of  peripheral 
motor  neurons  (462).  It  oc- 
curs in  disease  of  the  mus- 
cles, peripheral  nerves,  ante- 
rior horns  of  cord,  or  motor 
nuclei  in  brain  stem.  It  is 
never  functional,  but  may 
be  somewhat  simulated  by 
joint  disease.  Hypotonia  wnth- 
out  muscular  paralysis  or 
atrophy  occurs  in  cerebellar 
lesions,  tabes  and  other  ataxic 
conditions  (240). 


A  lesion  of  the  muscles  and 
often  of  the  thymus  gland. 


74 


Diagnostic 
Symptoms 
f254 
Hemiplegia 

(478-9) 
(Figs.  17-24;^ 


P 
A 
R 
A 

Y 
S 
I 

S 


i 


255 

Diplegia 
(478) 

256 


E 
X 

T  ^  Crossed 

E 

N 

T 


MOTOR  PARALYSIS  (Continued) 
Definition 
A  paralysis  with  exaggerated  tendon  reflexes 
of  one  lateral  half  of  the  body  and  extremi- 
ties limited  by  the  median  line  in  front  and 
behind.  It  is  partial,  if  limited  to  arm  and 
leg;  complete,  if  arm,  leg,  tongue,  palate  and 
face  are  all  involved.  In  some  cases  of  hemi- 
plegia there  are  slight  weakness  and  exag- 
gerated reflexes  on  the  other  side  of  the 
body  also,  especially  in  the  leg.  Symmetri- 
cal, bilateral  muscles,  which  have  a  com- 
mon function  and  a  bilateral  cortical  inner- 
vation, are  not  paralysed  :  at  most  tempor- 
arily weakened.  Such  are  the  ocular,  mas- 
ticatory, laryngeal,  respiratory,  diaphrag- 
matic, bladder,  rectal,  etc.,  muscles.  In 
cerebral  hemiplegia  certain  muscles  are, 
in  most  cases,  more  completely  paralysed 
than  others.  These  "predilection  muscles 
of  Wernicke"  are  the  trapezius,  the  ex- 
ternal rotators  and  adductors  of  the  upper 
arm,  the  triceps,  the  supinators  and  ab- 
ductors of  thumb,  the  exten.sors  of  the 
thigh,  the  flexors  of  the  leg  and  the  dorsal 
flexors  of  the  foot. 

A    double    hemiplegia    involving    both  sides. 
May  be  complete  or  partial  and  not  infre- 
quently  is   limited  to  the  legs,  or  the   face 
(facial  diplegia),  etc. 


paralysis 
(537-42) 

( Hemiplegia 
alternans) 

(Figs.  20-1) 

257 
Paraplegia 

(480) 
(Figs.  24-6) 


258 
Monoplegia 

(479) 
(Fig.  15) 

259 
Local 
paralysis 

(481') 
(Fig.  15) 


Significance 
A  lesion  of  the  contralat- 
eral central  motor  neu- 
rons (461).  H  e  m  i- 
plegia  is  usually  due  to 
a  cerebral  lesion,  but 
the  partial  form  may  be 
due  to  a  spinal  'esion, 
very  rarely.  Verj'  rare- 
ly, there  may  be  no 
lesion,  except  an  ex- 
treme local  anemia  or 
edema  of  the  brain  as 
in  nephritis  (hemiplegia 
sine  materia). 


A  lesion,  usually  but  not 
always  cortical,  of  the 
central  motor  neurons 
or  basal  nuclei  on  both 
sides. 


A  paralysis  of 
one  or  more 
homolateral 
cranial  nerves 
and  of  the 
contndateral 
arm  .'uid   leg. 


Always  due  to  a  lesion  involving  the  pyramidal  tract 
with  other  structures  in  the  brain  stem  (460)  ;  either  in 
the  medulla  (hypoglossal  hemiplegia  alternans — 
1290—1),  the  pons  (facial  hemiplegia  alternans — 1292), 
or  in  the  crus  cerebri  (motor  oculi  hemiplegia  alternans 
— 129.3).  The  nuclei,  or  the  neurons,  peripheral  or 
central,  of  the  cranial  nerves  are  involved  below  the 
decussation  of  their  central  neurons. 


A  symmetrical  par- 
alysis of  both 
sides  of  the  body. 
Usually  orly  i  n- 
volves  the  legs  and 
lower  part  of  body, 
but  may  involve 
the  arms  and  even 
both  sides  of  the 
face. 


May  occur  in  lesions  of  the  muscles  (dystrophies 
— 477),  or  of  the  peripheral  nerves  (neuritis — 
488-9).  or  of  the  spinal  cord,  or  brain  stem,  or 
even  of  the  cerebral  cortex  (bilateral  lesion). 
The  distinction  between  paraplegia  and  diplegia 
(255)  is  not  always  sharply  drawn.  In  general 
diplegia  is  applied  to  paralyses  of  cerebral  origin, 
paraplegia  to  those  of  spinal  or  peripheral  origin. 


•A  paralysis  of  one  ex-  May  be  due  to  lesion  of  motor  cerebral  cortex, 
tremity  only,  or  of  or  of  the  motor  nuclei,  or  of  the  peripheral 
one-half  of   the    face       nerves. 


only. 


May  be  due  to  lesions  of  muscles 
or  of  peripheral  nerves,  or  of 
spinal  cord,  or  rarely  of  motor 
cerebral   cortex,  or   functional. 


A  paralysis  limited  to  one  or  more 
muscles  of  the  face,  eye,  mouth, 
neck,  body  or  extremities.  Less 
than  a  whole  extremity. 

Inability  to  produce  vocal 
260  sounds.        Absence     of 

Aphonia  voice,  but  whispering  is 

[      (737-8)  i)Ossible. 

Methods  for  the  detection  of  paralysis  and  paresis  are  described  in  Chart  I  b. 
For  further  consideration  of  these  symptoms    and    of    the   diseases  in  which  they  occur,  see 
Chart  X. 


A  variety  of 
local  paralysis. 


Laryngeal  paralysis,  or- 
ganic or  functional. 


CHART  IVb 
Spasm 

Comprising  Numbers  245  to  247  and  263  to  276 


Analysi>  of  the  Symptoms  of  the  Case  (Semeiolo^^y! 


Diagnostic 
Symptoms 

r263 
Passive 
contrac- 
ture 
(Figs.  24-6) 


264 

Active 
contrac- 
ture 

(Figs.  15, 
17,  24-6) 


245 
T 
0 
N 
I 
0 

S 
P 
A 
S 


265 

Myotonia 
(590-603) 


266 
Rigidity 


267 

Convulsive 
tics 
(598) 


268 
Reflex 

spasm 


SPASM 
Definition 

A  continuous  contraction  of  long  duration  in 
which  the  muscles,  tendons  and  ligaments  have 
become  anatomically  shortened  and  cannot  be 
extended  by  force,  even  under  etherization. 
The  muscle'  fibers  are  degenerated,  while  the 
connective  tissue  of  the  muscle  is  hypertro- 
phied  and  usually  secondarily  contracted,  as  in 
other  newly  formed  connective,  or  scar,  tissue. 

A  continuous  contraction  lasting  weeks,  months, 
or  years,  which  can  be  overcome  by  force, 
either  with  or  without  etherization.  Muscles 
are  in  a  normal  condition  of  nutrition.  Most 
common  in  the  arms,  or  legs,  or  neck  muscles 
(torticollis).  The  active  contracture  of  a 
hemiplegia  is  usually  that  of  flexion  in  the  arm 
and  of  extension  in  the  leg. 


An  active  contracture  of  brief  duration  but  much 
longer  than  a  convulsive  tic.  It  may  occur  at 
the  commencement  of  voluntary  motion 
(Thomsen's  disease,  or  myotonia  congenita)  or 
may  be  excited  by  cold  (Eulenberg's  disease, 
or  paramyotonia  congenita).  It  is  frequent  in 
meningitis  and  tetanus  in  which  it  takes  many 
forms,  viz:  "retraction  of  head;"  "trismus," 
strong  closure  of  jaw;  "opisthotonos,"  arcliing 
of  body  backwards;  "pleurosthotonos,"  bend- 
ing of  body  to  one  side :  "emprosthotonos," 
arching  of  body  forwards  and  "orthotonos," 
holding  of  body  rigid  and  straight. 


An  active  contracture  of  such  mild  degree  that  it 
does  not  prevent  passive,  or  even  voluntary, 
motion  of  the  part,  although  rendering  it  diffi- 
cult   (paralysis   agitans,   etc. — 677). 


A  violent  spasm  of  momentary  duration.  If 
rapidly  repeated  it  must  be  classed  under  myo- 
clonus (270  and  .598  to  601).  If  painful  it  is 
called  "tic  douloureux"  (599). 


A  spasm,  usually  tonic,  caused  by  irritation  of 
some  sensory  tissue.  It  is  especially  common 
after  injury.  Many,  if  not  all,  of  these  reflex 
spasms  may  be,  really,  hysterical  and  can  be 
ci"-c-<^l  by  suggestion   (415).  j 


Significance 

Due  to  muscular  lesions 
and  to  degeneration  of 
the  peripheral  motor 
neurons  (462). 

Active  contractures  occur- 
ring in  hemiplegia  affect 
the  muscles  not  abso- 
lutely paralyzed.  When 
the  contracture  is  over- 
come by  the  application 
of  a  plaster  of  Paris 
splint,  the  muscles  often 
show  a  surprising  degree 
of  voluntary  motion 
when  the  splint  is  re- 
moved. These  contrac- 
tures depend  in  part,  on 
attempts  at  voluntary 
movements  and  on  asso- 
ciated movements,  but 
in  greater  part  on  reflex 
action  from  sensory  irri- 
tation ;  the  inhibitory  ac- 
tion of  the  brain  being 
cut  off  by  the  lesion. 
They  never  occur  in 
hemiplegia  in  tabetics 
and  in  any  case  can  be 
relieved  by  section  of 
the  po.sterior  nerve  roots. 
Such  contractures  are 
always  of  very  bad  prog- 
nosis as  to  recovery  from 
the  hemiplegia. 

Active  contracture  is  some- 
times due  to  paralysis 
of  antagonistic  muscles 
or  to  muscle  lesions. 

All  tonic  spasms  (not  in- 
cluding pas.sive  contrac- 
ture) are  due  to  a  func- 
tional disorder,  or  are 
reflex  (especially  in  chil- 
dren), or  are  due  to  irri- 
tation (chemical,  sen.sory 
or  vascular)  of  central 
motor  neurons  (461). 

Painful  cramps,  espe- 
cially in  legs,  of  the  na- 
iture  of  myotonia  or 
tics,  may  be  due  to  a  de- 
ficiency of  water  in  the 
system,  and  to  cold. 


7.S 


j^IAGNOSTIC 

Symptoms 

246  ^  269 

Gjnvulsion 

(571) 


i  270 
Myoclonus 
or 

convul- 
sive tics 

271 

Athetosis 
or  mobile 
spasm 
(574) 


SPASM  (Concluded) 
Definition 


Significance 


Violent  clonic  contractions  of  man}',  or  of  all  the, 
muscles  of  the  body. 


Successive  clonic  contractions  of  one  or  of  a  few 
adjacent  muscles.  Repeated  convulsive  tic. 
Most  common  in  the  face  muscles  (blepharo- 
spasm  (598). 


Slow,  worm-like,  rhythmical  movements,  often  "j 
associated  with  transitory  contractures 
(spasmus  mobilis),  of  fingers  and  wrists  and 
more  rarely  of  toes  and  ankles.  Hyperex- 
tension  is  the  predominant  action.  Usually 
unilateral,  but  may  be  bilateral.  Much 
more  common  in  children  than  in  adults. 
Muscles  of  the  neck,  face  and  of  other  parts 
of  the  body  are  not  infrequently  involved. 
It  never  occurs  in  completely  paralysed  mus- 
cles. 

272  Rapid,    irregular,    coordinated    but  purposeless 
Choreic  movements  caused  by  contraction  now  of  one 

move-  group  of  muscles,  now  of  another,  through- 

ments  out    the   body;  bilateral  or  unilateral  (hemi- 

Chorea  minor      chorea).     Cease  during  sleep.     They   often 

i^^^)  render  voluntary  movements  ataxic  and  are 

usually    associated    with    a    mild    degree    of 

paralysis  of  the  muscles  involved. 

273  Patient  performs  involuntarily  and  uncontrol- 
Chorea  ably  a  complicated  and  apparently  purpose- 
major  or  ful  movement.    Also  applied  to  a  coarse  tre- 
magna  mor   or    violent   oscillation    of  a  part  of  the 
(629)  body. 

274  Patient  frequently  performs  involuntarily,  and 
Habit  usually  unconsciously,  the  same  act.  Usually 

chorea  a  small  act. 

(627) 

275  Patient  is  compelled  by  some  power  within  him, 
Compulsory         which  he  cannot  understand  or  explain,  to 

acts    (218")       perform  certain  acts  against  his  will. 


Clonic  spasms  are  usually 
due  to  irritation  of  the 
cerebral  cortex,  but  may 
also  result  from  very 
exaggerated  reflexes 
(clonus). 


Lesion  is  usually  in  the 
caudate  nucleus  and 
putamen  of  contrala- 
teral hemisphere  and 
not  causing  complete 
paralysis.  May  occur 
in  diffuse  cortical  le- 
sions. 


Functional  disorders,  oc- 
curring in  the  neu- 
roses  and   in   insanity. 


Choreiform  movements, 
as  well  as  athetosis  and 
tremor,  may  occur  in 
lesions  of  the  corpus 
striatum. 


J 


276 

Associated 
move- 
ments 

(Synkinesis) 


Unintentional  muscular  contractions,  occurring 
when  movements  are  executed,  or  attempted 
in  muscles  not  directly  concerned  in  the  move- 
ment attempted;  often  the  corresponding 
muscles  of  the  opposite  side  of  the  body,  often 
those  of  the  face.  Such  associated  movements 
are  Bell's  phenomenon  (4,34),  Striimpell's 
tibialis  phenomenon  (435),  Babinski's  associ- 
ated movements  in  unilateral  paralysis   (436). 


In  such  cases  movements 
often  associated  to- 
gether, but  which  can  be 
easily  dissociated  volun- 
tarily in  health,  can- 
not be  dissociated  in 
disease  which  cuts  off 
voluntarv  action. 


Methods  of  detection  of  spasm  are  described  in  Chart  I  b. 

For  further  discussion  of  these  symptoms,  and   of   the  diseases   in   which   they   occur,   see 
Charts  XI  and  XII. 


79 


CHART  IVc 

Perversions  of  Motion 
Ataxia,  Loss  of  Skill,  Tremor 

Comprising  Numbers  248  to  250  and  280  to  294 


81 


Analysis  of  the  Symptoms  of  the  Case  Semeiology 

ATAXIA— LOSS  OF  SKILL 
[Ataxia  is  a  disorder  of  one  or  more  synergic   units    (simple  asynergia),   or   of    complex 
cerebellar  synergia  (integrative  asynergia),  or  a  disorder  of  the  cerebral  cortex  (apraxia).] 
Diagnostic 
Symptoms  Definition 


(280 
Motor 
ataxia 
(644) 
( dynamic 
ataxia) 
(Figs.  24-6) 

281 
Cerebellar 

ataxia 

(642) 

( static 

ataxia) 
(Figs.  19-26) 


Voluntary  movements  are  executed  in 
an  irregular  and  disorderly  manner, 
which  is  due  to  a  loss  of  the  co-ordi- 
nating power.  Rarely  associated 
with  decided  vertigo. 


Walking  and  standing  are  inco-ordi- 
nate,  but  other  acts  are  not,  or  only 
slightly  so.  Patient  executes  simple 
movements  of  his  legs  fairly  well 
when  lying  in  bed,  but  in  walking 
and  standing  he  lacks  synergy  of  the 
muscles  and  staggers  and  sways  like 
a  drunken  man.  Asynergia  major 
usually  associated  with  vertigo 
(392). 


Significance 
Is  due  to  a  loss  of  muscle  sense  (43) 
(deep  sensibility).  May  be  due  to 
lesions  of  peripheral  sensory  nerves, 
or  of  posterior  colimins  of  cord,  or 
of  brain  stem,  or  of  cerebral  cortex 
posterior  to  fissure  of  Rolando,  or 
may  be  toxic  (alcohol),  or  func- 
tional. 

Is  due  to  lack  of  muscular  synergy 
(42)  (asynergy).  Due  to  lesion  or 
functional  disorder  of  the  cerebellum 
or  its  tracts,  including  the  direct 
cerebellar  tract  in  brain  stem  or 
cord,  or  to  tumors  in  frontal  lobe  of 
brain  or  to  disease  of  ears  or  eyes, 
or  to  poisons  (alcohol,  etc.).  In 
lesions  of  the  cerebellar  hemisphere 
the  disorder  may  be  transitory;  in 
lesions  of  the  worm  it  is  more  per- 
manent. 


r 


282 
Apraxia 

(Fig.  IS) 


283 
Anarthria 

(737) 


284 
Dysarthria 

(738) 


285 
Dysphagia 

286 

Dysmasesis 
(554) 

287 
Astasia  and 

Abasia 
(652  and  795 
288 
Adiadocoki- 

nesia  {?>7) 
289 
Dysmetria 


Inability,  or  difficulty,  in  performing 
a  desired  and  accustomed  act  be- 
cause of  loss,  or  derangement,  of  the 
innervation  memories  concerned  in 
that  act  (Motor  aphasia,  agraphia, 
etc.).  The  voluntary  movements 
are  awkward  but  not  exactly  ataxic. 
The  patients  seem  to  have  lost  their 
initiative  to  action.  Sometimes  a  de- 
sired action  is  replaced  bv  a  different 
one  (231).  Loss  of  skill:  Asyner- 
gia minor. 

Absence  of  speech.  Speech  may  never 
have  been  acquired,  as  in  idiocy,  or 
may  never  have  been  acquired  on  ac- 
count of  deafness,  or  it  may  be 
voluntarily  restrained  for  a  purpose; 
or  it  may  be  more  or  less  involuntar- 
ily restrained,  as  in  insanity  or  hys- 
teria (Mutism  744-7). 

Such     difficulty     in     articulation     that  1  Occur  in 
speech      becomes      indistinct       and 
blurred,    but    is    probably    never    so 
great  as  to  cause  complete  anarthria 
(283). 


Lesion  of  the  cerebral  "common  paths" 
or  loss  of  innervation  memories, 
general  or  partial,  due  to  cortical  or 
subcortical  lesions  of  the  anterior  or 
posterior  central,  or  supra-marginal 
convolutions,  or  to  the  association 
fibers  connected  with  these  convo- 
lutions, or  to  functional  or  anemic 
disorders  of  cerebral  cortex.  (See 
page  37^. 


May  be  either  functional  or  organic 
and,  if  the  latter,  may  or  may  not 
be  due  to  lesions  in  the  peripheral 
organs  of  speech.  If  not,  it  is  called 
pure  motor  aphasia  or  aphemia. 


Difficulty  in  swallowing. 
Difficulty  in  mastication. 


Complete  inability  to  .stand  or 
but  legs  can  be  moved  freely, 
strongly,  when  lying  or  sitting. 


walk 
even 


Difficulty  in  repeating  a  movement 
rapidly,  especially  .supination. 

An  exaggerated  extension  of  the 
fingers  just  previous  to  grasping  an 
object. 

82 


esions  of  the  medulla  and 
pons  (bulbar  paralysis,  Figs.  21-3) 
and  of  the  cranial  nerves.  Also  in 
diphtheria,  hydrophobia,  mya.sthe- 
nia  gravis,  rarely  in  trichinosis 
and  frequently  in  hysteria  (globus 
hystericus).  These  symptoms  are 
due  to  a  combined  disorder  of  syn- 
ergic units  and  of  integrative  syn- 
ergia, or  to  nuclear  or  cranial 
nerve  paralysis,  or  are  functional. 
A  delusion  or  auto-suggestion,  which 
occurs  in  hysteria.  May  occur  rarely 
in  cerebellar  lesions. 

Occurs  in  lesions  of  a  cerebellar  hem- 
isphere, or  is  functional. 


Due  to  disorder  of 
(282). 


the 


synergic  units. 


250 
T 
R 
E 
M 
0 
R 


Diagnostic 
svmptoms 


TREMOR 
Definition 


290  Involuntary,    rhythmical    oscillation  or 

Passive  trembling  of  a  part  which  is  other- 

tremor  wise  at  rest. 

(646  and  647) 


291 

Intention 
tremor 
(645) 


An  involuntary  tremor  which  only 
occurs  when  a  voluntary  motion  is 
made,  or  is  willed  and  is  about  to 
be  made. 


292 

Nystagmus 
(640) 


293 

Fibrillary 
contrac- 
tion or 
fibrillation 
(641) 

294 

Myokymia 
(697) 


Significance 

Functional.       Occurs  in  paralysis  agi- 
tans,  weakness,  etc. 


Functional  and  organic.  Occurs  in 
neuroses  and  in  organic  diseases 
(disseminated  sclerosis).  It  is 
due  to  dissociation  of  synergic  units 
and,  therefore,  is  asynergia  rather 
than  tremor.  It  is  caused  by  lesions 
of  the  cerebellum,  of  the  putamen 
and  lenticular  nucleus  and  of  the  red 
nucleus  and  rubro-spinal  tract. 


An  involuntary  trembling  or  oscillation  of 
eyeball,  usually  horizontal,  rarely  verti- 
cal, very  rarely  rotatory.  Increased,  or 
only  occurs,  on  voluntary  motion  of  eye- 
ball, especially  on  extreme  deviation.  The 
rapidity  of  the  oscillations  varies  from  60 
to  200  per  minute ;  their  amplitude  from 
2  to  4  millimeters.  Nystagmus  may  be 
oscillatory  when  the  motion  in  each  direc- 
tion is  equally  rapid,  or  rhythmic  when  it 
is  quicker  in  one  direction  than  in  the 
other. 


Ocurs  espeially  in  lesions  of 
the  vestibular  and  other  nuclei 
in  the  pons,  Deiter's  nucleus 
in  the  cerebellum,  the  pos- 
terior longitudinal  bundle  in 
the  brain  stem,  in  disturb- 
ances in  the  semi-circular 
canals,  and  in  weakness  of 
ocular  muscles,  and  in  lesion 
of  ponto-cerebellar  angle, 
also  in  the  caloric  reaction 
(79),  and  in  cerebellar  disease 
(80).  It  is  due  to  dissociation 
of  synergic  units   (asynergia.) 


An  involuntary  contraction  of  a  bundle  Degeneration  of  those  multipolar  nerve 


of  fibers  of  a  muscle  of  short  dura- 
tion. When  many  occur  in  adjacent 
bundles  at  short  intervals,  waves  of 
contraction  run  over  the  muscle,  but 
do  not  cause  it  to  contract  as  a  whole. 


cells  in  the  anterior  horns  of  the 
spinal  cord  and  brain  stem  of  which 
the  motor  nerves  supplying  the  mus- 
cle are  the  axons.  Rarely  occurs  in 
traumatic  neuroses. 


A    fibrillary    twitching    of    the  muscles  Normal.     Exhaustion.     Following  ex- 
occurring  in  healthy  persons.  cessive  muscular  contraction  or  ex- 
posure to  cold. 


Methods  of  detection  of  perversions  of  motion  are  described  in  Chart  I  b. 
For  the  further  discussion  of  these  symptoms   and  of   the  diseases   in  which  they  occur,  see 
Chart  XII. 


83 


CHART  V 

Reflex  Activity 


ANALYSIS  OF  THE  SYMPTOMS    OF   THE    CASE  (SEMEIOLOGY) 
Definition,   Significance  and  Relationship  of  the  Symptoms  of  Disease. 


296  REFLEX  ACTS 


[297  CUTANEOUS  OR  SUPER-    1 
FICIAL  REFLEXES 

A  reflex  act  which  originates  from 
an  irritation  of  the  skin   (57). 


An  involuntary  movement  caused 
by  irritation  of  a  sensory  nerve 
or  terminal  organ.  Although 
not  the  result  of  a  conscious  in- 
tention, yet  these  acts  seem 
purposeful  and  usually  tend 
towards  the  protection  of  the 
body.  In  order  that  a  reflex 
act  may  take  place  there  musi 
be  a  comparatively  healthy  re- 
flex arc,  consisting  of  a  motoi 
nerve,  a  sensory  nerve  and 
some  gray  matter  connecting 
the  two;  or,  in  other  words, 
a  motor  neuron  and  a  sensory 
neuron  connected  together  di- 
rectly or  by  a  bridging  neuron. 
Reflex  acts  are  inhibited  and 
modified  by  inhibitory  im- 
pulses passing  down  from  the 
brain  along  the  so-called  inhib- 
itory fibers,  which  are 
also  the  central  motor  neu- 
rons :  the  pyramidal  tract 
(472-4,  811).  '(Figs.  19,  24). 


298  MUCOUS  MEMBRANE 
REFLEXES 

A  reflex  act  which  originates  from 
an  irritation  of  a  mucous  mem- 
brane (58). 

299  TENDON  OR  DEEP 
REFLEXES 

A  reflex  act  which  originates  from 
the  sudden  stretching  of  the 
fibers  of  a  muscle  (60-6). 

300  ORGANIC  REFLEXES 

A  reflex  act  afi"ecting  one  of  the 
viscera  of  the  body,  especially 
the  bladder  or  rectum  ( 1 ) . 

301  VASO-MOTOR  REFLEXES 

A  reflex  act  affecting  the  arterioles 

(59). 

302  PUPILLARY   REFLEXES 

A  reflex  act  affecting  the  pupil 
(25-8). 


The  conditions  in  which 
reflex  acts  are  disor- 
ordered  are  set  forth 
in  Chart  V  a. 


The  conditions  in  which 
the  pupillary  reflexes 
are  disordered  are  set 
forth  in  Chart  V  b. 


85. 


CHART  Va 

Cutaneous  or  |  Superficial  ^ Reflexes, 

Mucous  Membrane  Reflexes, 

Tendon  or  DeepIReflexes, 

Organic  Reflexes, 

Vaso-Motor  Reflexes 

Comprising  Numbers  303  to  328 


87 


Analysis  of  the  Symptoms  of  the  Case  (Semeiology) 


CUTANEOUS  REFLEXES 


Diagnostic 
Symptoms 

303 
Plantar 


304 

Babinsld's 

305 

Gordon's 


306 
Oppenhdm's 


307 
Gluteal 


307a 
Anal 

308 

Cremasteric 


309 
Umbilical 


310 

Epigastric 


311 

Interscapular 


312 

Corneal  or 
conjunctival 


Definition,    Elicitation    and 
Location  of  Reflex  Centers. 

Plantar  flexion  of  tlie  toes  associ- 
ated with  a  contraction    of    the 
tensor    fasciae    femoris     (Bris- 
saud's     reflex)    when    the   sole 
of  the  foot  is  irritated. 
(1st  and  2nd  sacral  segments.) 

Sluggish  extensive  dorsal  flexion 
of  the  great  toe  when  the  sole 
of  the  foot  is  irritated. 

Dorsal  flexion  of  the  great  toe 
when  deep  pressure  is  made 
through  the  calf  muscle  on  the 
deep  flexor  muscles  beneath  ;  the 
leg  being  completely  relaxed. 

Dorsal  flexion  of  the  great  toe 
elicited  by  firm  stroking  with  a 
hard  object,  or  finger,  just  he- 
hind  the  postero-internal  border 
of  the  tibia  from  above  down- 
wards ;  the  leg  being  completely 
relaxed. 

Contraction  of  the  buttocks  when 
the  skin  covering  them  is  irri- 
tated. 

(4th  and  5th  lumbar  segments.) 

Contraction  of  sphincter  ani  upon 

pin  pricks  of  anus. 
(5th  sacral  segment.) 

Drawing  up  of  the  testicle  when 
the  inner  side  of  the  thigh  is 
irritated. 

(1st  to  3rd  lumbar  segments.) 

Sudden  movement  of  umbilicus 
towards  the  side  of  abdomen 
irritated. 

(8th  to  12th  dorsal  segments.) 

Sudden  retraction  of  epigastrium 
when  the  hypochondrium  is 
irritated. 

(7th  to  9th  dorsal  segments.) 

Drawing  inwards  of  the  scapula 
when  the  skin  of  the  interscap- 
ular space  is  irritated. 

(Sth  cervical  to  Ist  dorsal  seg- 
ments.) 

Closing  of  the  eyelids  when  the 
cornea  or  conjunctiva  is  irri- 
tated. 

(Sth  to  7th  cranial  nucla.) 


Significance 

The  abnormal  reflexes,  Babinski,  Gordon  and 
Oppenheim  reflexes  and  ankle-clonus,  always 
indicate  disease  of  the  central  motor  neu- 
rons (461),  except  in  infants,  in  whom  these 
reflexes  (except  ankle-clonus)  may  be  pres- 
ent normally,  and  in  some  cases  of  hysteria, 
in  wliich  an  imperfect  ankle-clonus  may 
rarely  be  obtained.  The  Babinski  reflex  is 
most  reliable  in  a  diagnostic  sense.  The 
Oppenheim  reflex  is  sometimes  present  when 
the  Babinski  is  absent  and  vice  versa.  Ker- 
nig's  sign  indicates  meningitis  or  meningis- 
mus ;  it  is  an  important  but  not  certain,  diag- 
nostic sign   (320). 


Alterations  in  the  tendon  reflexes  are  of  very 
much  greater  diagnostic  value  tlian  are  those 
of  the  cutaneous  (except  the  Babinski)  re- 
flexes, which  are  in  many  cases  inconstant, 
probably  because  the  cutaneous  reflex  im- 
pulses may  possibly  pass  through  the  gray 
matter  of  the  brain  (cerebellum)  as  well  as 
through  a  wide  area  of  tliat  of  the  spinal 
cord. 


Diminution  of  reflexes  is  usually  of  little  diag- 
nostic value,  but  their  abolition  is  of  great 
value  and  may  be  due  to  a  destructive  lesion 
of  any  part  of  the  reflex  arc  (a  peripheral 
motor  neuron,  a  peripheral  sensory  neuron, 
or  a  central  bridging  neuron).  When  there 
is  a  lesion  of  the  peripheral  motor  neuron, 
atrophic  motor  paralysis  is  present  in  ad- 
dition to  the  loss  of  the  reflex.  When  there 
is  a  lesion  of  the  peripheral  sensory  neuron 
there  is  usually  a  sensory  paralysis  (anes- 
thesia, etc.)  in  addition  to  the  loss  of  the  re- 
flex. Diminution  or  abolition  of  reflex 
activity  (cutaneous  or  tendon)  may  occur, 
at  least  temporarily,  in  acute  diseases  or 
other  forms  of  irritation  of  the  central  motor 
neurons;  also  in  cases  of  shock,  exhaustion, 
coma,  narcotism  and  after  epileptic  fits, 
(except  Babinski)  ;  also  by  will  power 
and  by  voluntary  movements  of  the  muscles 
concerned;  also  (except  Babin.ski)  in  recent 
cases  of  complete  separation  of  the  brain 
from  the  reflex  centers  in  the  spinal  cord, 
and,  rarely,  from  increased  intracanial 
pressure,  also  frequently  in  fevers. 


88 


MUCOUS  MEMBRANE  AND  TENDON  REFLEXES. 


Diagnostic 
Symptoms 

313 
Nasal 


314 
Auditory-or- 

bicularis 

reflex. 


315 
Uvular 


316 
Pharyngeal 


317    ■ 
Ankle-clonus 


318 

Achilles 
reflex 

319 
Knee-jerk 


Definition, 
Location    of 


Elicitation  and 
Reflex  Centers. 


320 
Kernig's  sign 

321 

Dorsal  foot 
reflex 


322 

Elbow  and 
wrist 
reflexes 


323 

Maxillary 
reflex 


Sneezing  when  the  nasal  mem- 
brane is  irritated. 

(5th  to  10th  cranial  and  upper 
cervical  nuclei.) 

When  a  loud  noise  is  unexpectedly 
made  immediately  behind  the 
patient,  his  orbicularis  muscles 
contract.  This  reflex  cannot  be 
inhibited  and  may  serve  to  de- 
tect simulated  deafness. 

Raising  of  the  uvula  in  phonation 
or  upon  irritation  of  its  mucous 
membrane. 

(9th  to  10th  cranial  nuclei.) 

Retching     or    gagging    when    the 

pharynx  is  irritated. 
(9th  to  10th  cranial  nuclei.) 

Oscillation  of  the  foot  when  the 
ball  of  foot  is  pressed  quick- 
ly and  continuously  upwards. 

(5th  lumbar  and  1st  sacral  seg- 
ments. ) 

Sudden  plantar  flexion  of  foot 
when  the  tendo  Achillis  is 
sharply  struck,  patient  kneeling. 

(1st  and  2nd  sacral  segments.) 

Sudden  extension  of  knee  when 
the  ligamentum  patellae  is 
sharply  struck.  When  this  re- 
flex is  exaggerated  it  is  usually 
accompained  by  a  contraction 
of  the  adductors  of  the  opposite 
thigh,  or  even  by  knee-clonus 
(61). 

(2nd  to  4th  lumbar  segments.) 

Resistance  to  sudden  extension  of 
the  knee. 

Sudden  plantar  flexion  of  the  toes 
when  the  dorsum  of  the  foot 
over  the  4th  and  5th  metatarsal 
bones  is  struck. 

(5th  lumbar  and  1st  sacral  seg- 
ments.) 

Sudden  extension  or  flexion  of  el- 
bow or  wrist  when  the  corres- 
ponding tendons  are  sharply 
struck. 

(5th  to  7th  cervical  segments.) 

Sudden  closure  of  jaw  when  it  is 

sharply  struck  downwards. 
(5th  cranial  nucleus.) 


Significance 

The  abolition  of  the  knee-jerk  is  of  great  diag- 
nostic importance.  It  is  absent  in  tabes, 
neuritis  (multiple  and  crural),  acute  anterior 
iwliomyelitis  involving  the  extensor  cruris, 
Landry's  paralysis,  lesion  of  the  cauda 
equina  or  of  the  lumbar  enlargement,  during 
an  attack  of  family  periodic  paralysis, 
after  an  epileptic  attack  and  in  cases 
of  muscular  dystrophy  involving  the 
extensor  cruris  muscles.  It  is  usually  abol- 
ished in  Friedreich's  ataxia  and  combined 
sclerosis,  except  in  the  early  stages  when  it 
may  be  increased.  It  may  be  absent  in 
cerebral  compression  (tumor  or  meningitis) 
and  in  some  cases  of  cerebellar  disease,  and 
may  then  be  unilateral.  It  may  be  absent 
also  in  the  conditions  mentioned  in  the 
preceding  paragraph. 

Exaggeration  of  the  reflexes  may  be  due  to  a 
mild  inflammation,  or  to  any  irritation,  of 
any  part  of  the  reflex  arc.  Strychnine  in- 
creases reflex  activity  by  irritating  the  nerve 
cells  in  the  anterior  horns.  More  commonly, 
the  refle.xes  are  increased  by  any  lesion  of 
the  central  motor  neurons,  thus  cutting  off 
the  normal  inhibitory  influence  of  the  brain, 
and  are  then  associated  with  paralysis  of 
voluntary  motion.  The  presence  of  ankle- 
clonus,  the  Babinski  reflex  and  the  dorsal 
foot  reflex  indicates  a  lesion  of  the  pyramidal 
tract  much  more  certainly  than  does  an  ex- 
aggerated knee-jerk,  unless  the  latter  is 
associated  \vith  an  adductor  contraction. 
Very  commonly  the  reflexes  are  increased 
in  functional  diseases  (hysteria)  and  in 
nervousness. 


Innervation  of  the  muscles  not  concerned  in 
the  reflex  act  and  diverting  the  attention 
increases  reflex  activity  (reinforcement, 
68). 

The  paradoxical  reflex  is  of  no  diagnostic  im- 
portance. It  consists  in  a  contraction  of  the 
tibialis  instead  of  the  calf  muscles  when 
ankle-clonus  is  tested  for;  also  of  a  con- 
traction of  the  flexors  instead  of  the  exten- 
sors of  the  tliigh  when  the  knee-jerk  is 
tested  for. 

In  the  dorsal  foot-reflex  (Mendel-Bechterew) 
normally  there  is  either  no  reflex  or  a  dorsal 
flexion  of  the  toes,  but  in  cases  of  pyramidal 
tract  lesions  a  plantar  flexion  of  the  toes 
occurs. 


89 


ORGANIC  AND  VASO-MOTOR  REFLEXES. 


Diagnostic 
Symptoms 

324 
Bladder  or 

vesical 

reflex. 


325 
Rectal 
reflex 

326 

Ischemic 
reflex 

327 
Paralytic, 

hyperemic 

reflex 

(dermogra- 

pliia) 


Definition,     Elicitation      and 
Location    of    Reflex    Centers. 

The  retention  of  urine  in  the 
bladder  by  the  splrincter  reflex, 
the  expulsion  of  urine  by  the 
detrusor  reflex  and  the  syn- 
chronous relaxation  of  the 
sphincter. 

( Hypogastric  sympathetic  gang- 
glia.) 

Similar  to  that  of  the  bladder. 
(Hemorrhoidal  sympathetic  gang- 
lia.) 

A  sudden  pallor  of  the  skin  fol- 
lowing an  irritation  and  limited 
to  the  area  of  irritation. 

Congestion  of  the  skin  follow- 
ing the  ischemia  due  to  irrita- 
tion (taches  cerebrales  and 
dermographia). 


Significance. 

Inability  to  void  urine,  or  to  retain  it,  is  some- 
times due  to  nervousness  and  sometimes  to 
mechanical  obstruction  (enlarged  prostate  or 
stricture),  but  any  other  serious  disturbances 
of  the  organic  reflexes  indicate  organic 
disease  of  the  nervous  system.  It  never 
occurs  in  diseases  limited  to  the  peripheral 
nerves,  except  in  lesions  of  the  cauda 
equina,  and  rarely  in  cerebral  disease.  It  is 
most  common  in  spinal  disease:  sphincter 
paralysis  with  empty  bladder  and  constant 
dribbling  of  urine  in  lesions  of  lumbar  en- 
largement, and  detrusor  paralysis  with  dis- 
tended bladder  and  often  with  dribbling  of 
urine  in  lesions  above  the  lumbar  enlarge- 
ment.     (Fig.   28.) 

Vaso-motor  disturbances  cause  a  disturbance 
of  the  nutrition  of  the  part.  Diseases  which 
result  from,  or  are  associated  with,  disturb- 
ances of  the  vaso-motor  reflexes  are  dis- 
cussed in  Chart  XVII. 


328  By  irritation  of  the  skin  or  deeper  tissues  of 
Reflex  of  the  leg,  more  especially  by  firm  lateral  com- 
spinal  pression  and  powerful  flexion  of  the  foot 
Automatism  and  toes  there  results  a  flexion  of  all  the 
(Marie)  joints  of  the  leg  and  a  withdrawal  of  it  up- 
Defensive  wards. 
( Babinski ) 


Lesion  of  the  pyramidal  tract. 


The  methods  of  eliciting  the  various  reflexes  are  described  in  Chart  I  c. 

Diseases  in  which  the  reflexes  are  altered  are  discussed  in  Charts  X,  XIV,  XVI,  XVII. 


■.■•'.••.. 


90 


i:     I 


CHART  Vb 
Pupillary  Reflexes 

Comprising  Numbers  302  and  329  to  341. 


91 


Analysis  of  the  Symptoms  of  the  Case  .(Semeiology) 


302 
P 
U 
P 
I 
L 
L 
A 
R 
Y 

R 
E 
F 
L 
£ 
X 
E 
S 


Diagnostic 

Symptoms 
r329 
Pupillary 
reaction 
to  light 
(25) 


PUPILLARY  REFLEXES 
Definition,  Eucitation 
AND  Location  of 
Reflex  Centers 


330 

Pupillary 
reaction 
to  pain 
(28,  335) 

331 

Pupillary 
reaction 
to  accom- 
modation 
(27) 


332 

Argyll- 
Robert- 
son phe- 
nomenon 
(437,  891) 

333 

Immobile 
pupil 

(545) 


334 
Hemiopic 

reflex 

(26) 


Significance 


Pupil  contracts  when 
light  is  thrown  on 
retina  of  the  same 
eye  (direct  reflex), 
and  when  light  is 
thrown  on  retina 
of  opposite  eye 
(consensual  re- 
flex), and  dilates 
when  retina  is 
shaded  front  light 
(ciliary  ganglion). 


Pupil  dilates  in  pain, 
pincliing,  pin  pricks, 
etc.,  of  skin. 


The  direct  pupillary  reaction  to  light  is  abnormal  in 
lesions  of  any  part  of  the  reflex  arc  (optic  nerve,  cor- 
pora quadrigemina,  the  VVestphal-Edinger  cell  group  of 
the  motor  oculi  nucleus,  third  nerve  and  ciliary  gang- 
lion). If  the  lesion  is  in  front  of  the  optic  chiasm,  there 
will  result  blindness  of  the  corresponding  eye  with  loss 
of  the  direct,  but  preservation  of  the  consensual  reflex. 
If  the  lesion  is  back  of  the  chiasm  there  will  result  a 
partial,  never  complete,  loss  of  the  field  of  vision  of 
both  eyes,  and  both  the  direct  and  the  consensual  pupil- 
lary reflexes  will  be  preserved.  If  double  lesions  occur 
in  the  proximity  of  both  corpora  quadrigemina  and 
total  blindness  results,  both  the  direct  and  consensual 
reflexes  are  lost.  If  the  double  lesions  are  posterior  to 
the  corpora  quadrigemina  and  bilateral  heinianopia  or 
total  blindness  results,  and  both  the  direct  and  consens- 
ual pupillary  reflexes  are  preserved.  Both  these  reflexes 
are  absent  in  deep  .sleep,  narcosis,  shock,  coma,  epileptic, 
and  occasionally  in  hysterical,  attacks;  also  absent  in 
tabes,  in  many  cases  of  paresis  and  in  rare  cases  of 
syphilis  alone ;  absent  also  when  the  eye  is  under  the  in- 
fluence of  mydriatics  or  miotics.  A  careful  study  of 
tlic  pupillary  reflexes  will  serve  to  detect  many  cases  of 
malingering. 

This  reflex  may  be  deranged  in  lesions  of  the  cervical 
sympathetic  ganglia  of  the  same  side. 


Pupil  dilates  when 
I>atient  looks  at  a 
distant  object  and 
visual  axes  are 
parallel  and  con- 
tracts when  patient 
looks  at  a  near  ob- 
ject and  eyes  con- 
verge. 

Pupil  does  not  re- 
spond to  hght,  but 
does  respond  to  ef- 
forts at  accommo- 
dation. 

The  pupil  responds 
neither  to  light  nor 
accommodation,  but 
in  some  cases  may 
still  dilate  slightly^ 
on  irritation  of 
cervncal  s  y  m  p  a  - 
thetic. 

Pupil  contracts  when 
light  is  thrown  on 
the  unparalysed 
half  of  retina,  but 
does  not  contract 
when  light  is 
thrown  on  para- 
lysed half. 


The  pupillary  reaction  to  accommodation  is  absent  (cyclo- 
plegia)  in  lesions  of  the  third  nerve,  sometimes  after 
diphtheria,  occasionallv  in  alcoholism  and  when  the 
eye  is  under  the  influence  of  mydriatics  or  miotics, 
also  in  myopia  and  in  cases  of  deficient  convergence. 

The  Argyll-Robertson  phenomenon  occurs  in  almost  all 
cases  of  tabes  and  paresis  (in  many  of  these  cases  a 
degeneration  of  the  posterior  columns  of  the  cord  has 
been  found  at  autopsy)  and  very  rarely  in  cases  of 
syphilis  in  which  there  are  no  manifestations  of  either 
tabes  or  paresis  for  years  afterwards.  The  reverse  of 
the  Argyll-Robertson  phenomenon,  i.  e.,  the  preser- 
vation of  the  light  reflex  and  the  loss  of  the  accommo- 
dation reflex,  occurs  occasionally  in  diphtheritic  jjaral- 
ysis  and  has  been  found  associated  with  syphilis,  basal 
meningitis,  tumors  of  corpora  quadrigemina  and  mye- 
litis.    It  is  extremely  rare. 

Immobile  pupil  may  occur  in  lesions  of  the  optic  nerve 
or  tract  or  in  its  nucleus  or  in  that  of  the  third  nerve 
or  in  the  ciliary  ganglion  or  its  nerve.  It  may  also  be 
associated  with  ojihthalmoplegia  externa  or  interna  of 
both.  When  it  occurs  alone  it  is  due  to  lesion  in  the 
nucleus.  Immobile  pupil  also  occurs  in  tabes,  in  epi- 
lepsy, in  some  forms  of  hysteria,  in  fainting,  and  in 
katatonic  stupor. 

The  hemiopic  reflex  occurs  only  in  lesions  of  the  optic 
tract  or  geniculate  bodies  (homonymous  hemianopia) 
or  of  the  central  part  of  the  optic  chiasm  (bitemporal 
hemianopia).  The  existence  of  this  reflex  is  disputed 
by  many  obse^'^rs. 


92 


PUPILLARY  REFLEXES    (Concluded) 


Diagnostic 
Symptoms 

335 
Cilio- 

spinal 

reflex 

(465, 

1191-2) 


336 
Hippus 


337 
Westphal's 

pupil 

reaction 


338 
Paradoxical 

pupillary 

reflex 


339 

Mydriasis 

340 
Miosis 


Dehnition,  Eucitation 

AND  Location  of 

iReflex  Centers 


Significance 


341 

Unequal 
pupils  or 
anisocoria 


dilates     when  The   cilio-spinal    pupillary    reflex  is  absent  in  lesions    of 
skin     of     the      the  cervical  sympathetic,  and  in  many  lesions  of  the 


medulla  and  lower  cervical  and  upper  dorsal  region  of 
the  spinal  cord  (cilio-spinal  center — 465). 


Pupil 
the 

neck  on  same  side 
is  irritated,  (cer- 
\'ical      sympathetic 

ganglion)   or  when  Hippus  is  usually  associated  with  a  general  exaggeration 
cocaine   is   dropped      of  reflexes, 
in  the  eye. 

When  the  eye  is  sud-  Westphal's  pupillary  reaction  occurs  in   some  cases  of 
denly     exposed     to     tabes  and  in  paresis, 
light,    there   occurs 
a   series   of   altern-  The  paradoxical  pupillary  reflex  is  of  no  diagnostic  sig- 


nificance.    It  has  been  observed  in  tabes  and  in  paresis 
and  is  the  result  of  fatigue. 


ate  contractions 
and  dilatations  of 
the  pupil,  gradu- 
ally    growing    less  Mydriasis  may  be  irritative  or  spasmodic,  due  to  irrita- 


in  degree. 

When  patient's  eye- 
lids are  held  forc- 
ibly apart  and  he 
attempts  to  close 
them  he  not  only 
turns  the  eyeball 
upwards  (Bell's 
phenomenon")  but 
also  the  pupil  con- 
tracts. 

Pupil   dilates    ir  stead 


of 

upon 
light 
forts 


contracting 

exposure    to 

or    upon    ef- 

of      accom- 


modation. 


Dilated  pupils. 


Contracted  pupils. 


One  pupil  is  larger 
than  the  other 
when  the  eyes  are 
at  rest. 


tion  of  the  cervical  sympathetic  ganglion  or  nerve;  or 
may  be  paralytic,  due  to  paralysis  of  the  third  cranial 
nerve  or  the  ciliary  ganglion ;  or  may  be  due  to  both 
causes.  It  occurs  in  children,  and  on  taking  certain 
drugs  (mydriatics).  It  occurs  also  from  irritation  of 
the  cer\'ical  sympathetic  directly  by  incipient  lesions  in 
the  cervical  enlargement  of  the  spinal  cord  and  its  man- 
branes,  or  by  tumors  in  the  neck,  or  by  excess  of  car- 
bonic acid  in  the  blood  as  in  dyspnoea  and  indirectly 
by  strong  emotions  and  especially  by  pain ;  also  in  par- 
alysis of  the  sphincter  pupillae  (iridoplegia)  from  le- 
sions, such  as  optic  atrophy,  glaucoma,  lesions  of  the 
third  nerve  or  ciliary  ganglion,  which  break,  or  im- 
pair, the  refli-'x  arc,  and  which  usually  cause  more  or 
less  diminution  of  vision  and  a  deficient  perception  of 
light;  also  in  coma,  in  cases  of  increased  intra-cranial 
pressure,  and  in  some  other  cerebral  and  meningeal 
lesions,  especially  in  their  later  stages. 

Miosis  may  be  irritative  or  spasmodic,  due  to  irritation 
of  the  third  nerve  or  ciliary  ganglion ;  or  may  be  para- 
lytic, due  to  paralysis  of  the  cervical  sympathetic  gang- 
lion or  nerve,  or  may  be  due  to  both  causes.  It  occurs 
in  old  age,  in  deep  sleep,  or  on  taking  certain  drugs 
(miotics)  ;  also  from  irritation  of  the  third  nucleus  or 
nerve,  as  in  meningitis  in  early  stages  and  especially 
in  hemorrhage  into  the  pons ;  and  from  excessive  use  of 
accommodation,  as  in  watchmakers,  etc. ;  also  from 
paralysis  of  the  sympathetic  in  lesions  of  the  neck  and 
of  the  spinal  cord  (syringomyelia).  It  occurs  often  in 
tabes,  paresis,  iritis,  irritation  of  cornea  and,  tempor- 
arily, after  excision  of  the  Gasserian  ganglion. 

Anisocoria  occurs  in  many  conditions  and  is  of  little 
or  no  diagnostic  value. 


The  methods  of  eliciting  the  pupillary  reflexes  are  described  in  Chart  I  b. 
Disea.ses  in  which  these  reflexes  are  altered  are  discus.sed  in  Chart  XIV. 


93 


CHART  VI 

Disorders  of  Sensation 


ANALYSIS  OF  THE  SYPMTOMS  OF  THE  CASE  (SEMEIOLOGY) 
Definition,  Significance  and  Relationship  of  the  Symptoms  of  Disease. 


344  DISORDERS  OF  SENSA-        345  DIMINUTION 


1 


TION 

The  power  of  receiving  perceptions 
of  the  external  world  and  of  the 
occurrences  in  our  own  body 
(the  basis  of  all  knowledge)  is 
acquired  early  in  life.  The  na- 
ture of  the  process  is  entirely 
unknown,  but  it  rests  upon  the  . 
power  of  storing  up  merrtories 
and  of  recalling  them.  It  de- 
pends upon  the  integrity  of  the 
central  and  peripheral  sensory 
neurons  (463-4),  as  well  as  upon 
that  of  the  terminal  sensory  or- 
gans and  of  the  cerebral  cortex 
(47  to  56).  This  power  may  be 
diminished,  or  exaggerated,  or 
perverted  in  various  diseases. 


Either  no  perception  or  an  abnor- 
mally feeble  one  follows  a  sen- 
sory irritation  adequate  in  health 
to  cause  a  perception  (806,  811). 


346  EXAGGERATION 

An  unusually  strong  perception,  as 
compared  with  hralth,  follows 
any  sensory  irritation  (807). 


347  PERVERSION 

The  occurrence  or  modification  of  a 
perception  such  as  never  occurs 
in  health  (930). 


The    condiitons    under 
which   sensation   may 
be  diminished  or    in- 
creased are  set  forth 
in  Chart  VI  a. 


The    conditions    under 
which     sensation     is 
perverted  are  set 
forth  in 
Chart  VI  b. 


95 


CHART  Via 
Diminution  and  Exaggeration  of  Sensation 

Comprising  Numbers  345  and  346  and  348  to  372 


91 


Analysis  of  the  Symptoms  of  the  Case  (Semeiology) 


SENSATION 


Diagnostic 
Symptoms 

r348 
Anesthesia 
(complete)  or 
Hypesthesia 
( partial ) . 
(Superficial 
sensibility) 

349 

Analgesia  or 
Hypalgesia 


250 
D 
I 
M 
I 
N 
U 
T 
I 
0 
N 


Definition 

A  loss,  or  diminution,  of  the 
normal  sensibility  to  touch 
upon  adequate  irritation. 
Normal  sensibility  varies  in 
acuteness  in  dififerent  parts 
of  the  body  and  in  dilterent 
individuals. 

A  loss,  or  diminution,  of  the 
normal  sensibility  to  pain, 
which  in  heakh  varies  in 
different  individuals  and  in 
different  parts  of  the  body. 


Significance. 


350 

Thermic 

Anesthesia  or 
Hypesthesia 


A  loss,  or  diminution,  of  the 
sensibility  to  variations  in 
temperature.  Thir  loss  may 
be  more  marked  for  cold 
than  for  heat  and  vice  versa. 


351  Inability  to  distinguish   differ- 

Loss  of  pres-  ences  in  the  amount  of  pres- 

sure sense  sure  made  on  the  skin. 


352 
i  Loss  of  muscle 
and  joint 
sense  or 
Akinesthesia. 
(Deep 
sensibility) 

353 

Apallesthesia  or 
loss  of  osseous 
sense  or  vibra- 
tion sense. 

354 
Astereognosis 


Tnabilitv  to  tell  bow  stronglv  a 
muscle  is  contracted,  whether 
a  joint  is  flexed  or  ex- 
tended, or  where  an  extrem- 
ity is  situated  in  space.  A 
very  complex  sensation. 


Inability  to  feel  the  vibration 
of  a  tuning  fork  pressed 
firmly  on  the  skin. 


Inability  to  recognize  objects 
bv  the  sense  of  touch ;  anes- 
thesia not  being  present. 


355 

Deafness  or 
Anakusia  or 
Hypakusia 

356 

Anosmia  or 
Hyposmia 

357 

Ageusia  or 
Hypogeusia 


Ix)ss.  or  diminution,  of   sense 
of  bearing. 


Diminution  of  sensibility  may  be  due  to 
disease  of  the  terminal  end-organs,  or  to 
a  destructive  lesion  either  of  the  peri- 
pheral sensory  neurons  (464),  (in  wliich 
case  all  forms  of  sensibility  are  abolished 
over  an  area  usually  couiciding  with, 
but  smaller  than,  the  distribution  of  the 
peripheral  nerve,  and  the  reflex  acts  in 
the  same  part  are  also  abolished)  ;  or  of 
the  sensory  central  neurons  (463),  (in 
which  case  frequently  all  forms  of  sensi- 
bility are  not  abolished,  and  the  anes- 
thetic area  does  not  correspond  to  the 
area  of  distribution  of  a  nerve,  and  the 
reflex  acts  in  the  part  are  not  abolished). 
Sensiliility  is  abolished  in  coma,  nar- 
cosis and  often,  apparently  only,  in  hys- 
teria. A  broad  zone  of  analgesia  and,  more 
rarely,  of  anesthesia  also,  about  the  body 
occurs  in  locomotor  ataxia :  "tabetic 
cuirass."  The  anesthetic  area  may  coin- 
cide with  the  distribution  of  a  peripheral 
nerve  or  with  that  a  nerve  root  (peri- 
pheral lesion)  ;  or  with  the  distribution  of 
several  nerve  roots  (spinal  lesion)  ;  or  the 
area  may  involve  one-half  the  body: 
called  hemianesthesia  (cerebral  lesion  and 
hysteria).  Anesthesia  of  one  side  of  the 
face  and  of  the  opposite  arm  and  leg, 
"crossed  hemianesthesia,"  occurs  in  lesions 
in  the  tegmentum  of  the  pons  and  in  the 
restiform  body  in  the  medulla.  Anesthesia 
may  involve  some  portion  of  the  body  sup- 
plied by  small  branches  of  many  different 
nerves,  such  as  a  hand,  a  foot,  a  leg,  a 
foreann,  etc.,  and  be  .sharply  limited: 
"stocking  and  glove  variety"  (hysterical). 
(Fig.  3.1^ 

Analgesia,  thermic  anesthesia  and  apalles- 
thesia may  be  due  to  lesion  of  the  central 
gray  matter,  or  of  the  antero-lateral  as- 
cending tract,  of  the  cord  (Fig.  26)  or  of 
the  peripheral  nerves  or,  very  rarely,  in 
hy.steria.     (Fig.  26.) 

Astereognosis  always  indicates  a  lesion  of 
the  cerebral  cortex.     (Fig.  15.) 


Loss,  or  diminution. 
of  smell. 


Loss,   or  diminution,   of   sense 
of  taste. 


Anakusia.  anosmia,  ageusia  and  blindness, 
of  sense  may  be  due  to  a  lesion  of  the  .sensory 
terminal  organ,  of  the  sensory  nerve  or 
tract,  or  may  be  functional.  But  these 
symptoms  may  occur  in  .so  many  condi- 
tions unconnected  with  the  nervous  sys- 
tem that  they  may  have  very  little  diagnos- 
tic value  in  nervous  diseases. 


9,S 


SENSATION  (Continued) 


Diagnostic 
Symptoms 

358 

Blindness  or 
Anopsia  or 
Amaurosis 

359 

Amblyopia 


Los 


Definition. 
of  vision. 


360 
Hemeralopia 


361 
Nyctalopia 


362 
Hemianopia 


Decided  impairment,  but  not 
complete  loss,  of  vision, 
especially  for  colors  in  the 
early  stages.  Usually  in 
such  cases  the  field  of 
vision  is  made  small  by  the 
loss  of  more  or  less  of  its 
periphery  or  by  scotomata. 

A  condition  in  which  the  pa- 
tient sees  better  in  a  dim 
light    than    in    a    bright  one 

(day  blindness). 

A  condition  in  which  the  pa- 
tient sees  well  in  a  bright 
light  but  is  almost  blind  in 
a  dim  one  (night  blindness). 

Loss  of  one-half  of  the  field  of 
vision. 


c  ^ 


Homonymous  Loss  of  the  same  half  in  both 
fields. 


Nasal  Loss  of  the  nasal  half  in  each 

or  either  field. 

Bi-temporal      Loss   of   the   temporal  half   in 
both  fields. 
In  almost  all  cases  of  hemian- 
opia a  limited  area  of  cen- 
tral vision  is  preserved. 

363  Loss  of  an  homonymous  quad- 

Tetartanopia  '"^^t  of  both  fields  of  vision. 

or  Ouadrantic 

Hemianopia 


364 

Achromatopsia 
or  color  blind- 
ness.     Hemi- 
chromatopsia 

365 

Dissociation 
of  sensation 


Inability  to  distinguish  the 
different  colors  from  each 
other  either  throughout  the 
whole,  or  in  one-half,  the 
field  of  vision. 

Loss  of  some  forms  of  cu- 
taneous sensibility  (usually 
for  pain  and  temperature) 
with  preservation  of  others 
(tactile).     (Figs.  24-7.) 


Significance 

Hemeralopia  associated  with  a  central  sco- 
toma for  green  and  red  is  not  uncom- 
mon in  tobacco  smokers.  In  them,  when 
the  pupil  is  dilated  in  a  dim  light,  the 
healthy  part  of  the  retina  can  act.  Tliis 
condition  is  quite  different  from  snow- 
blindness,  where  the  retina  is  exhausted 
by  too  bright  and  too  long  continued 
light. 

Nyctalopia  is  at  times  associated  with  con- 
genital retinitis  pigmentosa,  with  cor- 
tical (peripheral)  cataract  and  with  other 
defects  in  the  eye,  and  from  exhaustion. 

Hononymous  hemianopia  is  due  to  a  lesion 
of  the  optic  tract  posterior  to  the  chiasm, 
of  the  geniculate  bodies,  the  optic  fascicu- 
lus or  the  median  surface  of  the  occipital 
lobe  of  the  opposite  side  of  the  brain 
(lips  of  calcarine  fissure).     (Fig.  16) 

Bi-temporal  hemianopia  is  due  to  a  lesion 
of  the  central  part  of  the  optic  chiasm. 
Nasal  hemianopia  is  due  to  a  lesion  of 
the  lateral  margin  of  the  optic  chiasm. 
Bi-nasal  hemianopia  cannot  result  from 
one  lesion. 

Tetartanopia  is  due  to  a  lesion  of  the 
upper  lip  of  the  contralateral  calcarine 
fissure  if  it  be  a  lower  quadrant  of  the 
field  of  vision  and  of  the  lower  lip  of  this 
fissure  if  it  be  an  upper  quadrant:  very 
rarely  to  a  partial  lesion  of  the  geniculate 
bodies  or  optic  fasciculus.     (Fig.  16.) 

Achromatopsia  may  be  due  to  a  congenital 
defect  or  to  defective  education  or  may 
be  the  early  stage  of  a  gradually  devel- 
oping blindness  or  amblyopia.  Due  to 
mild,  not  completely  paralysing,  lesions 
of  any  portion  of  the  visual  tract  in  the 
broad  sense. 

Dissociation  of  sensation  always  indicates 
a  lesion  of  the  central  gray  matter 
(syringomyelia)  or  of  the  spino-thalamic 
tracts,  or  more  rarely  at  the  ponto-cere- 
bellar  angle  of  the  pons  at  the  level  of  the 
auditory  nerve.  It  occurs  associated  with 
motor  paralysis  of  the  opposite  side  of  the 
bodv  in  some  cases  of  Brown-Sequard's 
paralysis. 


99 


SENSATION   (Concluded) 


Diagnostic 
Symptoms 

''366 
Hyperesthesia 


346 

E 
X 
A 
G 
G 
E 
R 
A 
T 
I 
0 
N 


367 
Hyperalgesia 

368 

Thermic  Hyper- 
esthesia or 
Hyperalgesia 

369 
Hyperosmia 

370 
Hypergeusia 

371 
Photophobia 

1^372 
Hyper  akusia 


Definition 

Increased  tactile  sensativeness. 
An  unusually  slight  touch 
can  be  perceived.  A  very 
rare  and  even  doubtful  con- 
dition. It  is  usually  em- 
ployed when  a  touch  causes 
an  unusually  great,  even 
painful  sensation,  where  hy- 
peralgesia or  haphalgesia 
(380)  would  be  a  better 
term. 

Increased  sensitiveness  to  pain. 


Significance 


Exaggeration  of  sensibility  of  all  kinds  is 
usually  functional.  More  rarely  it  is  the 
result  of  an  irritative,  rather  than  a 
destructive,  lesion  of  the  central  or 
peripheral  sensory  neurons.  It  occurs 
in  strychnine  poisoning  and  tetanus. 
Hyperesthesia  occurs  as  a  zone  at  the 
upper  limit  of  the  anesthesia  in  many 
spinal  lesions,  and  on  the  same  side  of 
the  body  as  is  the  lesion  in  Brown- 
Sequard's  paralysis.  It  is  usually  asso- 
ciated with  increased  reflex  activity. 


Increased,   even  painful,  sensi- 
tiveness to  heat  or  cold,  or  n.    .     ,    ,  ■      ■      r       .  •       ,  , 
...                                     '        Photophobia   is    functional,    or    due    to  eye 

strain,   or  to   inflammation   of    some  part 
of    the    eye,    or    optic    nerve,    or  cerebral 

Increased,  even  painful,   sensi-  * 

tiveness  to  odors. 


Increased  and  unpleasant   sen- 


sitiveness to  taste. 

Increased    and    painful    sensi 
tiveness  to  light. 

Increased,  even  painful,   sensi 
tiveness  to  sounds. 


Hyperakusia  is  functional,  or  due  to  ear 
diseases  affecting  the  labyrinth,  or  to 
cerebral  conditions  causing  hyperemia  of 
the  labyrinth  (meningitis,  encephalitis, 
tumors,  etc.)  and  to  spinal  affections. 


Methods  for  the  detection  of  these  conditions  are  described  in  Chart  I  c. 
Diseases  in  which  these  conditions  occur  are  discussed  in  Chart  XIV. 


100 


CHART  VIb 

Perversions  of  Sensation 

Comprising  Numbers  347  and  374  to  392 


101 


Analysis  of  the  Symptoms  of  the  Case  (Semeiology) 


Diagnostic 
Symptoms 

^374 
Pain 

(Figs.  33, 
38) 


375 
Paresthesiae 


,v6 
Failure  of 

localization. 

Topoanesthesia 

377 
Allocheiria 


SENSATION 

Definition 

Is  an  unpleasant  sensation  not  felt  in 
perfect  health,  except  in  cases  of 
injury.  It  varies  greatly  in  intensity. 
It  presents  different  qualities,  such 
as :  tearing,  cutting,  burning,  throb- 
bing, darting,  etc.  It  may  be  diffuse, 
or  felt  in  a  small  area(localized),or 
may  run  along  a  nerve  trunk  (radi- 
ating), or  may  run  half  way  or  en- 
tirely about  the  body  or  an  extrem- 
ity (girdle),  or  it  may  be  felt  in  an 
area  which  is  itself  anesthetic  (an- 
esthesia dolorosa.)  Pains  may  vary 
as  to  time  of  occurrence,  some 
showing  a  distinct  periodicity  (ma- 
laria, neuralgia  and  migraine), 
some  occur  at  menstrual  epochs. 
Some  headaches  occur  in  morning 
(uremic),  others  in  afternoon 
(ocular)  and  others  towards  even- 
ing and  at  night  (syphilitic). 
Some  pains  are  increased  by  pres- 
sure (neuritis  and  neuralgia)  while 
some  are  diminished  liy  it  (lead 
colic ) . 

Curious  sensations  rarely  felt  in  per- 
fect health,  usually  unpleasant  but 
not  severe  enough  to  be  called  pain. 
They  are  numbness,  tingling,  formi- 
cation, heat,  cold,  heaviness,  tired 
feeling,  hunger,  etc. 

When  a  cutaneous  sensation  is  felt  but 
cannot  be  localized. 


378 

Double  sen- 
sation and 
Polyes- 
thesia 

379 

Paradoxical 
sensation 

380 
Haphalgesia 

381 

Retardation 
of  conduc- 
tion of  pain 

382 

Persistence 
of  sensation 


When  an  irritation  is  not  felt  at  the 
point  of  contact,  but  at  a  corres- 
ponding point  on  the  opposite  side 
of  bodv. 


Significance 

Perversions  of  sensibility,  especially 
pain  and  paresthesiae,  are  often 
lunctional  and  are  often  due  to 
irritation  (pressure,  chemical,  in- 
flammatory, etc.)  of  central  or  peri- 
pheral sensory  neurons.  Radiating 
and  girdle  pains  are  usually  due  to 
lesions  of  the  nerve  roots.  Anes- 
thesia dolorosa  is  due  to  a  lesion  of 
the  central  end  of  a  sensory  neuron 
which  has  been  destroyed  below  this 
point  and  therefore  can  conduct  no 
sensations  from  below  up  to  the 
brain. 

Although  pain  may  be  felt  as  peri- 
pheral it  may  be  of  central  origin 
and  due  to  lesions  of  central  neu- 
rons within  the  brain  or  cord.  On 
the  other  hand  pains  due  to  lesions 
in  the  abdominal  viscera  may  be  re- 
ferred to  remote  part<;  of  the  hnrlv 
or  the  head  (referred  pains — 953). 


Failure  of  localization  may  be  func- 
tional but  usually  results  from 
lesions  of  the  peripheral  sensory 
neurons   (tabes). 

.'Mlocheiria  occurs  in  hysteria,  very 
rarely  in  tabes,  hemiplegia  and 
sclerosis. 

Polyesthesia  occurs  only  in  tabes  and 
in  hysteria. 

Paradoxical  sensation  has  been  met 
with  in  a  number  of  spiiial  .and 
cerebral  diseases,  but  is  without 
diagnostic  significance. 


When  one  contact  gives  rise  to  two 

distinct    sensations    (double  sensa-  Haplialgesia  occurs  in  hysteria, 
tion)  or  more  (polyesthesia). 


The    quality    of    thermic  sensation  is 
reversed,  a  hot  bodv  feels  cold  and 


vice  versa. 


Retardation  of  coiuluction  of  pain 
occurs  only  in  lesions  of  [Peripheral 
sensory  neurons  (tabes  or  multiple 
neuritis),  and  is  therefore,  a  very 
imiwrtant   diagnostic   symptom. 


A  slight  tactile  impression  from  cer-  Persistence  of  sensation  occurs  in 
tain  objects,  but  not  from  others,  is  lesions  of  the  peripheral  sensory 
felt  as  intense  pain.  neurons  (tabes). 

The  sensation  of  pain  is  not  felt  until  Binocular  diplopia  is  due  to  a  weak- 
an  appreciable  interval  after  the  ness  of  one  or  more  of  the  external 
time    of  contact.  muscles  of  one  eye,  or  to  displace- 

ment  of   one   eyeball;    so  that  the 
The  sensation  continues  an  unusually      image    does    not    fall    on    identical 
long  time  after  the  irritation  causing      spots  in  the  two  retinae, 
it  has  ceased  to  act. 

102 


SENSATION   (Concluded) 


P 
E 
R 
V 
E 
R 
S 
I 
0 

^<   388 


Diagnostic 
Symptoms 

383 
Binocular 

Diplopia 

(818) 

384 

Monocular 
Diplopia 
or    Poly- 
opia (880- 
4) 


C 
O 

n 

c 
1 
u 
d 
e 
d 


385 

Metamor- 
phopsia 

386 
Micropsia 

387 
Macropsia 


Tinnitus 
Aurium 

389 
Parakusis 


390 
I'arosmia 

391 
Parageusia 

392 
Vertigo 


I. 


Definition 

Two  separate  visual  perceptions  of  the 
same  object,  the  perception  from 
the  normal  ej-e  (true  image)  being 
more  distinct  than  that  from  the 
abnormal  eye   (apparent  image). 

A  condition  in  which  objects  appear 
double  or  multiple,  e\ei\  when 
looked  at  with  one  eve  alone. 


A  condition  in  which  objects  appear 
distorted. 


A  condition  in  which  everything  looks 
much   smaller   than   normal. 


Significance 


A  condition  in  which  everything 
much  larger  than  normal. 


looks 


A  sound  of  ringing,  roaring,  whistl- 
ing, etc.,  in  ears  or  head. 

Perversions  of  hearing,  such  as  hear- 
ing tones  incorrectly  or  hearing  bet- 
ter when  other  loud  noises  are 
present  at  the  same  time,  or  hear- 
ing sounds  or  words  for  which  there 
is  no  external  cause  (hallucina- 
tion). 

The  perceptions  of  abnormal  odors 
or  of  those  for  which  there  is  no 
external  cause   (hallucination). 

The  perception  of  abnormal  tastes 
or  of  those  for  which  there  is  no 
external   cause    (hallucination). 

A  feeling  as  if  the  person  (sub- 
jective) or  as  if  surrounding  ob- 
jects (objective)  were  whirling 
about,  or  both. 


Diseases  in  which  these  conditions  occur  are  discussed 

103 


Monocular  diplopia  may  occur  in  hys- 
teria, in  cases  of  double  pupillary 
opening,  in  anomalous  refraction 
(incipient  cataract),  and  irregular- 
ities in  the  cornea. 

Metamorphopsia  may  occur  in  hys- 
teria, also  in  astigmatism  (re- 
iracrive)  and  in  displacement  of  the 
retinal  elements  (retinal)  wliich 
may  ocur  in  retinitis,  choroiditis, 
and  in  detachment,  or  tumor,  of 
retina. 

Micropsia  may  occur  in  hysteria,  in 
paralysis  of  accommodation  and, 
with  distortion,  when  the  retinal 
elements  are  spread  apart  (recent 
choroiditis  or  retinitis). 

Macropsia  may  occur  in  hysteria,  in 
spasm  of  accommodation  and.  with 
distortion,  when  the  retinal  elements 
are  crowded  together  ( atrophic 
stage  of  retinitis  and  choroiditis). 

Tinnitus  aurium,  parakusis,  parosmia 
and  parageusia  occur  in  lesions  of 
the  terminal  organ  of  the  un- 
cinate gyrus,  and  in  insanity  and 
functional  disorders.  They  may 
constitute  the  aura  of  an  epileptic 
attack. 

Vertigo  may  be  functional  (hysteria, 
neurasthenia,  traumatic  neuroses)  ; 
or  may  depend  on  changes  in  the 
cerebral  circulation,  especially 
anemia  and  hyperemia  (cardiac  and 
arterial  diseases,  congestion  in  por- 
tal or  systemic  circulation,  galvan- 
ism of  head  or  neck),  or  toxic  (to- 
bacco, morphine,  alcohol,  some  di- 
gestive disturbances,  etc.)  :  or  may 
depend  on  diseases  of  the  cerebel- 
lum and  its  tracts,  or  of  the  ear  or 
eye.  It  is  the  principal  symptom 
in  Meniere's  disease  f aural  ver- 
tigo). Vertigo  is  closely  associated 
with  vomiting.  In  vertigo  associat- 
ed with  lesions  in.  or  pressing  upon, 
a  cerebellar  hemisphere,  external 
objects  seem  to  whirl  in  the  direc- 
tion away  from  the  injured  hemi- 
sphere in  both  conditions,  but  the 
subjective  vertigo,  usually,  is  away 
from  the  injured  hemisphere  in  case 
the  lesion  is  within  it  and  towards 
it  when  the  lesion  is  external  and 
presses  upon  the  hemisphere. 

in  Charts  XXIV  and  XV. 


CHART  Vila 

Electrical  Examination 

Comprising  Numbers  393  to  403 


105 


Analysis  of  the  Symptoms  of  the  Case  (Semeiology) 

Definition,  Significance  and  Relationship  of  the  Symptoms  of  Disease 


393 

ELECTRICAL 
REACTION 
OF  MUSCLES 
AND  NERVES 

(70-3) 
Nerve  fibers 
respond   to 
changes  in 
intensity  of 
both  the  far- 
adi'  and  the 
galvanic  cur- 
rents.    The 
dianges  in 
intensity  are 
best  brought 
about  by 
making  and 
breaking   the 
current. 
Muscle  fibers 
respond  only 
to  the  galvanic 
current.     The 
muscl-  re- 
sponds to  the 
faradic  current 
only  in  virtue 
of  the  nerve 
fibi-rs  supplied      ■ 
to  it.     When 
these  nerve 
fibers  are  de- 
generated the 
muscles  can  no 
longer  resiiond 
to  Ihe  faradic 
current.     Both 
nerves  and 
muscles  have 
points  on  the 
body    surface; 
the  so-called 
motor  points 
(see  figures  1  to 
fi)   from  which 
they  are  most 
readily  excit- 
able.  There- 
fore, in  testing 
a  nerve  or 
muscle  by 
electricity  the 
electrode  (pos- 
itive or  nega- 
tive) is  plac*^! 
on  the  corre- 
sponding 
motor  point. 
(70-3L 


Name 

OP  THE 

Reac- 
tion 
394 

Normal 
excita- 
bility 
(473) 


Tis- 
sue 

Test- 
ed 


3"J5 
Dimin- 
ished 
excita- 
bility 


3'.H1 
Exag- 
gerated 
excita- 
hilicy 


397 
Reac- 
tion  tt 
degen- 
eration 
(472) 


N 

E 
R 
V 

E 

A 
N 

D 

M 
XJ 

S 

c 

L 
E 


N 
E 
R 
V 
E 


M 
V 
S 
C 
L 
E 


Reaction 

TO 

Faradism  . 

Contraction 
present    to 
a  strength 
of  current 
wliii-h   is 
normal  for 
the  nerve 
and  muscle 
tested. 

Contraction 
present  but 
it    requires 
an  unusually 
strong 
current  to 
produce  it. 


Contraction 
present  to 
an  unusually 
weak 
current. 


Gradual 
loss  of 
excitability 
which  be- 
comes com- 
plete in 
about 
two  weeks 
after  injury 
or  onset  of 
the  disease. 


<  Jr.ndu.-tl 
loss  of 
excitability 
which  be- 
comes com- 
plete in 
le.ss  than 
two  weeks 
after  in.jiiry 
or  onset  of 
the  disea.se. 


Reaction  to  Galvanism 

AND 

FoRMiLA  OF  Galvanic  Reaction 

Neg.Cl.C.  Pos.CI.C.  Pos.Op.C.  Neg.Cl.Tet. 
is  the  normal  formula,  or  in  other  words 
Neg.Cl.C.  occurs  with  the  weakest  cur- 
rent that  will  cause  an.v  contraction. 
Pos.CI.C.  occurs  with  a  little  stronger 
current.  Pos.Op.C.  occurs  with  a  still 
stronger   current. 

The  explanation  of  the  above  formula 
is  as  follows :  The  weakest  current 
that  will  cause  any  contraction  of  the 
muscle  will  do  so  when  the  negative 
electrode  is  on  the  motor  point  and  the 
current  is  closed.  (Neg.Cl.C.)  A 
more  powerful  contraction  will  take 
place  when  a  .stronger  current  is  used 
and  then  there  will  also  be  a  contrac- 
tion when  the  current  is  closed  and 
the  positive  pole  is  on  the  motor  point 
(Pos.CI.C).  A  still  more  powerful 
current  causes  a  contraction  when  the 
current  is  opened  and  the  p<isitive  elec- 
trode is  on  the  motor  point  (Pos.Op.C). 
With  such  powerful  currents  and  the 
negative  pole  on  the  motor  points  there 
results  a  tetanus  or  continuous  con- 
traction when  the  current  is  closed. 
(Neg.Cl.Tet.)  ;  so  that  the  muscle 
cannot  relax  to  contract  again  when 
the  current  is  opened.  There  is.  there- 
fore, in  health  no  reaction  correspond- 
ing to  "Neg.Op.C" 


Nr)   reaction. 


.\fter  the  first  two  weeks  the  muscle 
responds  to  unusually  feeble  galvanic 
currents  and  the  normal  formula  is 
reversed  ;  tlie  positive  pole  being  more 
potent :  Pos.CI.C.  Neg.Cl.C.  Pos.Op.C. 
Neg.Op.C  (which  last  reaction  never 
occurs  in  health). 

It  is  usual  to  express  the  formula  for 
the  normal  reaction  and  for  the  reac- 
tion of  degeneration  in  the  German 
language  in  which  Kathwle  means  the 
negative  electrode  and  .\nmie  means 
the  po-sitive  electrode.  Tlie  usual  form- 
ula is  K.C.C,  A.C.C..  A.O.C,  K.CTe. 
The  reaction  of  degeneration  is 
A.C.C..  K.C.C,  A.O.C  K.O.C 
The  essence  of  the  normal  formula  is 
K.C.C  >  A.CC  The  essence  of  the 
formula  of  the  reaction  of  degeneration 
is  A.CC  >  K.C.C. 


Character    Significance 

OF  THE 

OF  the 

Contrac- 

Reaction 

tion 

Normal 

excitability 

shows  a 

noi"mal 

condition 

of  muscle 

and  nerve. 

Diminished 

excitability 

occurs  in 

many  dis- 

eases and 

conditions 

(thick  skin), 

Quick. 

especially  in 

lesions  of 

the  central 

motor  neu- 

rons and  is 

not  of  much 

value  in 

diagnosis. 

Exaggerated 

excitability 

is  a  rare 

condition.  It 

occurs  in 

nervous 

persons  with 

moist  skins 

and  in  tetany. 

The  reaction 

of  degenera- 

tion  proves 

None. 

that  the  peri- 

pheral motor 

neurons  are 

degenerated 

and  that  re- 

covery will 

Sluggish. 

either  never 

take  place. 

Tlie 

or  will  be 

sluggish 

very  slow. 

character 

The  lesion 

of  the 

must  be 

muscular 

either  in  the 

<-on  tract- 

perii)heral 

ion    is 

uer\es  or 

the   most 

nerve   roots 

charac^ 

or  in  the 

teristic 

anterior 

thing  in 

horns  of  the 

the   react- 

spinal cord 

ion  of 

or  in  the 

degen- 

motor nuclei 

eration. 

in  the  brain 

stem. 

106 


ELECTRICAL  REACTIONS   (Concluded) 


Name 

OF   THE 

Reaction 


398 
Partial 
reaction 
of  degen- 
eration 


399 
Myas- 
thenic 
reaction 
(553) 


\    400 
Myo- 
tonic 
reaction 
(613) 


401 

Neuro- 
tonic 
reaction 


Reaction       Reaction 
Tissue        to  to 

Tested    .  Far.'^dism     Galvanism 

Contractions    present,  but  1 
Nerve         require  unusually  strong  I 
currents,    whether    far-  j 
adic  or  galvanic. 

Contractions  Contractions  i 

present  only  present  to       j 

Muscle    'o  unusually  unusually        ! 

strong  cur-  weak  cur-      | 

rents.  rents 


J 


Formula  of 
Galvanic 
Reaction 


Sluggish. 


Either  the 
normal  form 
ula,  or  the 
formula  of  the 
reaction  of 
degeneration, 
or  a  combina- 
tion of  the  two 
may  be  pres-      Sluggish 
ent'.  A.C.C. 
may  equal 
K.C.C. 


Character 

OF  THE     Significance 
contrac-        of  the 
tion  Reaction 

The  signifi- 
cance of  this 


Quick  or 


Nerve 

and 

Muscle 


Nerve 
and 

Muscle 


Contractions 
quickly  grow 
less  strong 
and  soon 
cease  under 
rapidly 
repeated 
excitation. 

Continuous 
tonic  con- 
traction 
lasting 
some  time 
after  the 
electrical 


Xormal 


Normal 


Quick ; 

grows 

rapidly 

weaker 

and 


Curious 

wave-like 

contractions 

occur  and 

last  after 

electrical 

stimulation 


stimulation       has  ceased, 
has  ceased. 

Nerve  Unusually  excitable.  Te-  j 
tanic  contraction  persists  I 
after  electrical  stimula- 1 
tion  has  cea.sed. 


Positive  pole 
is  about 
equally  as 
potent  as  the 
negative. 
Hence  the 
formula 
A.C.C.  =  K.C.C. 


Continues 
usually  a 
long  time 
and  has  a 
wave-like 
character. 


reaction  is 
the  same  as 
that  of  the 
reaction  of 
degeneration, 
except  that  it 
indicates  the 
lesion  is  less 
severe  and 
that  all  the 
nerve  fibers 
are  not  de- 
generated. 

Occurs  only 
in  myas- 
thenia gravis 

(554). 


Occurs  in 
Thomsen's 
disease 
(611). 


402 

Reaction 
of  com- 
pletely 
degenerated 
muscle 
(70  to  73) 


I  Muscle    Normal.  Normal. 

Muscle    None.  None. 


Normal. 


None. 


Continuou? 


None. 


Occurs       in 
hysteria, 
amyotrophic 
lateral 

sclerosis  and 
chronic  bul- 
bar paralysis. 

Muscle  fibers 
are  entirely 
degenerated 
and  recovery 
is  impossible. 


403 

Electrical 

reaction 

of  the 

Optic  and 

Auditory 

Nerves 


The  optic  nerve  responds  to  the  galvanic  f-urrent  witli  a  .«ensation  of  light,  the  color  of  which 

varies  with  the  pole  employed. 
The  auditory  nerve  responds  with  a  loud  sound  when  the  negative  electrode  is  placed  in  or  near 

the  meatus  and  Uie  current  closed  and  with  a  faint  sound  when  the  positive  pole  is  used  and  a 

stronger  current  broken.     These  reactions  are  withoait  diagnostic  importance. 
The  negative  electrode  placed  in  front  of  the  ear  causes  a  nystagmus  towards  the  ear  teste<l  when 

the  current  Ls  close<l  and  in  the  opposite  direction  when  the  current  is  broken.     The  positive 

clectrmie  causes  nystagmus  in  exactly  the  reverse  direction. 


In  cases  of  disease  in  which  the  caloric  test  ( 79)  is  absent  and  in  which  the  electric  te.st  is 
present,  it  is  fairly  certain  that  the  lesion  is  in  the  labyrinth  and  not  in  the  nerve.  If  there  is  no 
response  to  either  the  caloric  or  the  electric  te.st  tlv   lesion  is  in  the  nerve  or  its  nucleus. 

107 


CHART  Vllb 

Erb's  Motor  Points  for  Electrical  Examination  of 

Nerves  and  Muscles 


The  motor  points  are  the  areas  upon  the  surface  of  the  body  at  wliich  the  individual  nerves  and 
muscles  can  be  most  easily  excited  by  electricity.  For  the  nerves,  these  points  coincide 
with  those  at  which  the  nerve  lies  most  superficially  or  where  it  can  be  pressed  against  a 
resisting  tissue;  for  the  muscles,  they  lie  over  the  point  of  entrance  of  the  nerve  into  the 
muscle. 

Comprising  Figures  1  to  5 


109 


ERB'S  MOTOR  POINTS 


M.  frontalis 

Upper  brunch  of 
facial 
M.  corrug. 
supercil. 

M.  orbir.  palpebr. 

Muscles  of  the  ( 

DOse  1 

M.  zygomatici 

M.  orbicul.  oris-( 

Middlt:  hnmch  of 
facial 

M.  luasseter 

M.  levator  nienti 

M.  quadr.  meiiti 

M.  triang.  nieuti 

■iV.  h)j}>nijlass. 

Lower  bniiich  of 

facial 

^i.  platysnia 

niyoiilr-s 

Muscles  of  Xhv  J 

root  of  tonguf  ( 


M.  oniohvoideus 


y.  thoracic,  anter. 
(M.  pector.) 


Region  of  central 
convolutions 


Region  of  the 
iliird  frontal 
convohit  ion . 

M.  temporalis 

Upper  branch  of 
facial  in  front 
of  ear 

S.  facialis 

X.  aiiriculo.  post. 
Middle  branch  of 

faiial 
Loner  br.  of  facial 
M.  splenius 
H.  sternocleido- 

luastoideus 
iV.  accessonii.i 

M.  levator  anguli 

sea  puke 
M.  cucuUaris 

N.  dnrs.  scapulce 


N.  axillnris 


N.  thoracic,  long. 
(M.  serratus 
antic,  niflj.) 


JV.  phrenicvs 


.Suprascapular  Plexus 

point.     (Erb's  point.       brachialis 
M.   deltoid.,    biceps, 
brachial,  intern,  and 
supinat.  long.) 

Fig.  1 


U.  lficrp»  <caput 


M   n^xor  cnrpiulii; 


M.  f1<.*x.  (lijiitor. 
niuii.  prorund 


M.  flex,   digltof.  «itb- 
lim.  (•liKitlllet  lllj 


M   palman*  l>re?, 
M,  abaitctordigill 

M,  «.-»or  digit-  min. 

M.  (.pponi-u*  dlRli, 

111  lit 


M.  tumbilcftles 


M.  supinator  lonpos 
M.  pronator  teres 
M    flex  Ciirpl  radi.iliB 


AVrc  mujf  iiJonUon/uji 
M.  bicep*  brBibli 
M,  lirach   inii'iniis 


M    flixoT  <IlKltoT  "utrlinj.  , 
M.  flex,  pollici^  lODgvis 

M    abductor  polUr  bret, 
M.  opponeD*  po)llcl» 

M   flet.  poll.  bre», 

M   ftflductor  i«Vi<:  bre». 


Fig.  2 


110 


ERB'S  MOTOR  POINTS  (Concluded) 


^.  rmdialu 
M.  brtcbUl.  Intern 

M.  aupinttor  long. 
51.  radial,  csi.  long. 
U.  radUI.  eit.  bre*. 

M  exlfn-ur  iliglt.  ronimunts 
M,  exteosor  indfcii 
M   Bbductor  polllc  long. 
M.  eilfrDsor  polllc  brev. 


M   int«r*«  dor^ftl 


M  iric«p»  (caput  longimi) 


M.    triceps   (caput    «x- 
tero.) 


Fig.  3 


.M    ulnir  fiiem. 
M.  supioat.  bret. 


M.  eiten.*.  dlgiti  miaiOL 
M   eitens.  Indicia 


M.  eit«ii9.  poll   loD^ 


M.  abdnct.  dtgit  mlD. 


M.  adJucEormagnus 
M.  addiict,  Inn^s 


M    Tx^tui  lalernj9 


M.  esteos.  digit   cunim. 
long 


U.  peronein  brer 


M.  extonsor  balliicis 

lODg- 


M.  iaierotMei  dorules 


M.  tensor  faacie  Iat« 

M.  sarlorliu 
~  M.  quadricrpa  feuioria 
JI.  rectus  remorij 

vastua  extcnua 


M.  (lastrocaem.  rxitr 
M   peroaeus longua 


flexor  hallucU  toag. 


M,  eitcos  digit.  < 


M.abdutior  dlgiti  miB. 


Fig.  4 


a  [  M  giut«uj 


AWr.  UcMadicut 
H.  bicepa  tem.  (cap.  lung.) 
M.  bleep*  fern.  (cap.  brev.j 


if.  prnneui 
H.  gKstrnciiOiu.  icap.  exlero.)      f — • 

M.  Mleu^ 


M,  flexor  hallucis  longus 


masiaiM 


Iductor  niagiiua 
.M    svniitendinosu* 
M   vtiiKiieiiibniuiMu* 


f>'    llllUXllM 


M   gistrocnem.  (cap  lou) 
M.  solmis 


CHART  VIIc 


ERB'S   DIAGRAM    SHOWING  THE   EFFECTS  OF  INJURY  OF  A  NERVE 


\<^^*^mLm 


GiJ>'< 


t  (Galvanic 
5:^1  ■«  ar&dic 


f    a»  w«K. 


tieatlh       '°t?f<TJr  y3Hhi;».Jft-oKf,r&tiojofniu^kCirrU^      feSiSS. 


Ga^lvdnic 


glfjLrab 


V  Ji  JO  To         JO  40         SO  to  70       T»  9*~ 

Fig.  6 


®W3  ■ 


Charts  Illustrating  the  Reaction  of  Degeneration 

The  star  (*)  indicates  the  incidence  of  a  paralysing  lesion  in  the  domain  of  the  peripheral 
neuron.  Voluntary  motion  is  lost  at  once.  During  the  first  two  weeks  there  is  slight  diminu- 
tion of  the  galvanic  excitability  of  muscle;  there  is  also  rapid  diminution  of  the  faradic  excitability 
of  muscle  and  of  the  galvanic  and  faradic  excitability  of  nerve,  which  are  completely  lost  at  the 
end  of  the  second  or  third  week.  During  the  second  week  there  is  rapid  increase  in  galvanic  ex- 
citability of  muscle  and  the  response  to  the  positive    pole    becomes    greater    than  to  the  negative. 

Chart  1  represents  the  reaction  in  a  case  terminating  in  recovery.  During  the  sixth  week 
(indicated  by  the  cross  X)  regeneration  begins.  The  increased  galvanic  excitability  of  the  muscles 
gradually  diminishes  until  it  becomes  normal  and  the  poles  are  reversed  so  that  the  negative 
response  is  again  greater  than  the  positive.  Voluntary  motion  returns  first,  then  the  galvanic 
and  faradic  excitability  of  the  nerve,  and  last  of  all,  the  faradic  excitability  of  the  muscles. 

Chart  2  represents  the  reaction  in  a  case  terminating  in  atroph)'  and  cirrhosis  of  the  muscle. 
The  galvanic  excitability  of  the  muscle  is  increased  and  the  poles  are  reversed,  as  before.  The  de- 
cline in  galvanic  excitability  continues,  however,  until  the  end  of  the  second  year,  when  it  is  en- 
tirely lost.  Voluntary  motion,  and  the  electrical  reactions  of  both  muscles  and  nerve  are  per- 
manently destroyed. 


113 


CHART  VIII 
Analysis  of  the  Cerebro-Spinal  Fluid 

Comprising  Numbers  405  to  414 


115 


Analysis  of  the  Symptoms  of  the  Case  (Semeiology) 


Character- 
istics 


ABNORMAL  CEREBRO-SPINAL  FLUID 


''405 
Tension 


404 
A 
B 
N 
0 
R 
H 
A 
L 


406 

Red  or 
reddish 
yellow 
color 

407 
Qoudy 

408 

Clear  with 
delicate 
coagulum 

409 
Celhilar 

elements 

and 

bacteria 


Methods  of  Testing 
Can  be  roughly  estimated  by 
the  rapidity  of  flow  of  fluid 
through  the  canula,  whether 
in  drops  or  a  stream;  more 
accurately  by  the  height  to 
wliich  the  fluid  rises  in  a  ver- 
tically held  glass  tube  con- 
nected by  a  short  rubber  tube 
with  the  canula.  A  stopcock 
on  the  canula  adds  to  the  ac- 
curacy by  preventing  the 
escape  of  much  fluid  and  the 
consequent  lowering  of  the 
tension.  The  fluid  in  the  tube 
rises  and  falls  with  the  res- 
piration. An  additional 
more  rapid  and  stronger  pul- 
sation indicates  a  basilar 
aneurism. 

By  sight. 
Hematoidin   crys-" 

tals      may      be 

seen    imder  the 

microscope. 


Significance 
A  low  or  very  rapidly  diminishing  tension  has 
no  diagnostic  meaning,  except  as  indicat- 
ing an  obstruction  to  the  communication 
of  the  fluid  in  the  ventricles  with  that  of 
the  vertebral  canal,  as  in  closure  of  the 
foramen  of  Magendie. 

A  high  tension  means  increased  intra-cranial, 
or  intra-spinal,  pressure  caused  by  an  in- 
creased amount  of  cerebro-spinal  fluid  or 
by  a  foreign  bod)'  within  the  cerebro-spinal 
cavity.  It  occurs  in  tumors,  abscess, 
hydrocephalus,  hemorrhage,  acute,  sub- 
acute and  some  cases  of  chronic  and  serous 
meningitis,  also  in  cerebral  edema  (nephri- 
tis, anemia,  etc.).  acute  infectious  diseases 
and  some  other  conditions. 


By  sight. 

Pus  cells  under  the  microscope. 

( Polymorphonuclear  leucocytes ) 

By  sight. 


Fresh  blood  in  the  fluid  may  be  the  result  of  puncture  of  a 
blood  vessel,  in  which  case  it  is  most  abundant  in  the  fluid 
first,  drawn,  usually  coagulates,  and  settles  quickly  on  cen- 
trifugalization.  Or 

May  be  the  result  of  hemorrhage  into  the  ventricles  or 
membranes    (Hematorhachis,  hematoma,  aneurism,  etc). 

An  increase  of  cellular  elements  in  the  fluid  is 
usually  the  result  of  an  acute  or  sub-acute 
meningitis'.  In  some  cases  of  acute  menin- 
gitis, however,  the  fluid  may  be  clear. 


Tuberculous  meningitis,  usually. 


Fluid  soon  after  withdrawal 
should  be  centrifugalized. 
Tube  should  be  emptied 
quickly  and  from  its  walls 
and  bottom  sediment  should 
be  sucked  in  and  out  of  a 
capillary  tube,  well  mixed 
and  spread  on  two  clean 
slides.  One  slide  should  be 
stained  by  Gram's  method 
for  bacteria,  especially  a 
smear  of  the  fine  pellicle 
found  in  some  clear  fltiids.  in 
which  tubercle  bacillii  are 
found  in  90%  of  the  cases 
and  the  other  by  Wright's 
blood  stain  for  cellular  ele- 
ments.        Or 

The  fluid  (not  centrifugalized), 
10  parts,  can  be  mixed  with 
1  part  of  a  solution  consist- 
ing of  methylene  blue  0.2%, 
glacial  acetic  acid  4.0%.  and 
water  to  100%,  and  counted 
in  a  Thoma-Zeiss  chamber. 
Or 

Rinse  out  the  white  counting 
pipette  with  glacial  acetic 
acid,  draw  in  well-shaken 
freshlv  drawn  cerebro-spinal 
fluid  and  count. 

116 


The  normal  cerebro-spinal  fluid  shows  under 
these  conditions  1  to  5  cells  in  a  field  of  the 
microscope.  If  there  are  more  than  6  to  8 
cells  in  a  field  it  indicates  a  meningitis. 

If  the  cells  are  mainly  polymorphonuclear 
leucocytes  it  indicates  epidemic  cerebro- 
spinal, or  purulent,  meningitis,  or  rarely  an 
acute  tuberculotis  meningitis :  broadly 
speaking,  an  acute  infectious  meningitis. 

If  the  cells  are  mainly  or  entirely  lymphocytes 
it  indicates  a  tuberculous  meningitis,  or 
cerebro-spinal  svphilis.  or  paresis,  or  tabes, 
or  aaite  anterior  poliomyelitis,  encephalitis 
or  convalescence  from  any  form  of  acute 
meningitis;  broadly  speaking  a  chronic  in- 
fectious meningitis. 

If  echinococcus  cysts  or  hooklets  are  present, 
thev  indicate  the  presence  of  an  echinococ- 
cus cyst. 


ABNORMAL  CEREBRO-SPINAL  FLUID  (Concluded) 


Character- 
istics 

410 
Sugar 


A 
B 
N 
0 
R 
M 
A 
L 

C 
E 
R 

E 

B 
R 

0 

I 

s 
p 
I 

N 
A 
L 

F 
L 
U 
I 
D 


411 
Albumen 


412 
Globulin 


Method  of  Testing 
By  Haines'  test  or  other  tests. 


Significance 

Not  of  much  significance,  but  the  sugar  nor- 
mally present  is  diminished,  usually,  in 
meningitis  and  in  some  other  conditions. 


Two  c.  c.  of  the  fluid  mixed  with    Normally    not    more    than    %%    is  present. 


10  c.  c.  of  Esbach's  fluid  is 
centrifugalized  during  one 
hour  in  a  conical  tube  grad- 
uated to  0.1%. 


Usually  increased  in  meningitis  and  tu- 
mors. A  diminution  in  the  amount  usu- 
ally indicates  a  progressive  space-oc- 
cupying disease.  Of  little  diagnostic 
significance. 


Indicates 
meningitis, 
acute  ante- 
rior polio- 
myelitis, 
encephalitis, 
cerebro- 
spinal 
syphilis, 
paresis,  tabes, 
rarely  a  brain 
tumor. 


414 

Colloidal 
gold  test 
(Lange) 


Two  c.c.  of  a  saturated  solution  of  chemically  pure  neutral 
ammonium  sulphate  should  be  placed  in  a  test  tube  and  one 
c.  c.  of  the  cerebro-spinal  fiuid  should  be  gently  run  upon  its 
top.  If  the  reaction  is  positive,  within  3  minutes,  a  grayish 
white  ring  should  form  at  the  junction  of  the  two  fluids. 
At  the  end  of  one-half  hour,  the  surface  of  the  ring  should 
show  a  delicate  network.  Best  seen  by  indirect  illumina- 
tion. (Nonne-Apelt  test.) 
Or 

Boil  slightly  1  volume  of  the  cerebro-spinal  fluid  with  5 
volumes  of  a  10%  butyric  acid  solution,  add  1  volume  of  a 
normal  solution  of  sodium  hydroxide,  reheat  and  allow  to 
cool.  If  a  flocculent  percipitate  forms,  the  reaction  is  posi- 
tive.    (Noguchi  test.) 

The  globulin  test  is  of  little  or  no  value,  if  the 
fluid  contains  red  blood. 


The  reaction  is  positive  in  90%  of  cases  of  paresis  and  in  60% 
of  cases  of  tabes. 

In  cerebro-spinal  syphilis  both  the  cerebro-spinal  fluid  and  the 
blood  usually  give  a  positive  reaction.  In  other  cases  of 
sypliilis  (without  meningitis)  the  reaction  is  usually  nega- 
tive with  the  cerebro-spinal  fluid,  but  positive  vrith  the 
blood. 

This  test  is  to  be  regarded,  and  used,  only  as  an  additional  or 
confirmatory  test.  It  is  of  much  value  in  syphilitic  diseases 
of  the  central  nervous  system,  especially  tabes  and  paresis. 
It  is  positive  in  about  80%.  of  the  proved  cases. 


413 

This  test  can 

Positive 

only  be  per- 

Wasser- 

formed  in  a 

mann 

laboratory 

reaction 

by  an 

expert. 

L 


This  test  can 
only  lie  per- 
formed in  a 
laboratory 
by  an 
expert. 


(Note) — In  the  examination  for  cellular  elements  (409),  it  is  important  to  always  check  up  the 
type  of  the  cells  present  and  the  presence  of  blood  cells  by  centrifuging  the  cerebro-spinal 
fluid  and  staining  a  drop  of  the  sediment  by  Wright's  stain.  It  is  especially  important  to 
thus  diff'erentiate  resistant  red  blood  corpuscles  from  small  lymphocvtes;  so  that  the  former 
may  not  be  counted  with  the  latter,  and  in  interpreting  the  results  of  the  globulin  and  col- 
loidal gold  tests;  both  of  which  tests  are  vitiated  by  the  presence  of  blood.  This  method  gives 
also  a  surprisingly  accurate  estimation  of  the  number,  as  well  as  of  the  type,  of  cells  present. 


117 


CHART  IX 
Special  Syndromes  and  Anatomical  Terms 


Comprising  Numbers  415  to  465 


119 


Syndromes  and  Special  Symptoms  of  Disease 

Syndrome  Definition 

415  Occur  usually  in  self-conscious  females  of  an  emotional  nature.     Lack  of  inhibi- "i 
Hysterical       tion    and    great    susceptibility    to  suggestion.     Desire  to  excite  admiration  and 

symp-  sj-mpathy  and  wonder.      Mental  instability.      Globus  hystericus  (416).     Spinal, 

toms  inguinal,    (or    ovarian)    and    other    tenderness.     Great    variety    of    symptoms 

(1076)  (especially  subjective)  wluch  cannot  be  explained  by  any  organic  lesion. 
Glove  and  stocking  form  of  anesthesia  or  hemianesthesia  and  concentric 
contraction  of  the  field  of  vision  are  common  symptoms,  but  the  patient  is  usually 
ignorant  of  their  existence  until  they  are  discovered,  or  more  probably  suggested, 
by  the  physician.  This  glove  and  stocking  form  of  anesthesia  rarely  occurs  also 
in  multiple  neuritis  and  syringomyelia.  Exaggerated  reflexes  but  no  ankle- 
clonus  or  only  pseudo-clonus.  Never  a  Babinski  reflex.  Motor  paralyses, 
tremors,  contractions  and  convulsions  are  not  uncommon.  Transference  of 
hemianesthesia  can  be  affected  in  some  cases  by  suggestion  or  by  the  apphca- 
tion  to  the  anesthetic  areas  of  metal  discs,  especially  those  made  of  gold.  The 
anesthesia  of  the  fingers  does  not  prevent  delicate  acts  being  done  by  them  with 
eyes  closed.  Such  patients  when  tested  and  the  anesthetic  area  is  touched  often 
answer  "no"  at  the  moment  of  contact  (Janet's  test,  48).  Many  other  symp- 
toms do  not  seem  to  be  real  but  rather  seem  to  be  imaginary  and  may  result  from 
liallucinations  or  delusions  or  more  probably  are  the  result  of  suggestion:  auto- 
or  foreign.  Probably  many  of  the  hysterical  symptoms  come  into  existence  as 
the  result  of  the  physician's  careful  and  minute  examination  or  repeated  ex- 
aminations (foreign  suggestion).  Many  other  symptoms  in  addition  to  those 
above  mentioned  are  met  with  in  hysteria.  Among  the  more  important  are: 
blindness,  coma,  aphonia,  astasia  and  abasia,  anorexia,  vomiting  and  regurgita- 
tion of  food,  tympanites,  phantom  tumors  and  false  pregnancies,  hemoptysis, 
anuria  and  melauuria.  Many  of  these  symptoms  are  pure  "fakes."  They  even 
drink  their  own  urine,  so  great  is  their  desire  to  excite  wonder. 

416  The  feeling  of  a  lump  or  ball  behind  the  upper  end  of  the  sternum  wliich  interferes 
Globus  both  with  swallowing  and  breatliing.  The  sensation  often  commences  in  the 
Hystericus       epigastrium  and  rises  to  the  base  of  the  neck  and  remains  there ;  the  patient  not 

(1076)         being  able  to  get  it  up  or  down.     It  may  be  caused  by  a  spasmodic  contraction  of 
the  muscles  of  oesophagus  or  throat. 


Signifi- 
cance 


Hys- 
teria 
(1076) 


417 

Hystero 
genie 
areas  (1076) 


Spots  scattered  over  the  body,  but  usually  in  the  left  inguinal  region,  where  Light 
pressure  or  irritation  will  cause  more  or  less  \'iolent  hvsterical  attacks. 


418 

Hystero- 
frenic 
areas  (1076) 


Spots  scattered  over  the  body,  but  usually  in  the  left  inguinal  region,  where  firm 
and  continued  pressure  will  cause  the  arrest  of  an  existing  hysterical  attack. 


419 

Lasegue's 

symp- 
tom (1076) 

420 

The  epi- 
leptic 
aura 
(1061, 

575,  849) 


A  condition  in  which  the  patient  cannot  move  an  anesthetic  extreinity  when  her 
eyes  are  closed,  but  can  move  it  readily  when  she  opens  her  eyes  and  looks  at  it. 


The  aura  is  a  symptom  (warning)  which  occurs  before  the  attack  in  about  half  the 
cases  of  epilepsy.  It  may  be  remote  or  immediate.  The  former  is  often 
called  "a  prodromal  symptom"  and  occurs  hours  and  days  before  the  attack.  It 
consists  usually  in  an  emotional  change  (irascibility,  etc.),  changes  in  the  amount 
of  sleep,  of  food  taken,  in  sexual  desire  and  vasomotor  phenomena.  Much  more 
characteristic  and  important  is  the  immediate  aura  wliich  occurs  a  fraction  of  a 
minute  before  the  attack.  This  aura  may  be  "psychic"  Canxietv,  anger,  joy, 
dreamy  states,   special   thought  or  memory,  etc.),  or  a  "sensory   lialludnation" 


Epi- 
lepsy 
(575,  849, 
1061) 


120 


SYNDROMES  AND  SPECIAL  SYMPTOMS  OF  DISEASE  (Continued) 

Syndrome  Definition 

which  may  be  visual  (blindness,  hghts,  colors  (red),  elaborate  false  visual  per- 
ceptions, etc.)  or  auditory  (deafness,  noises,  and  false  auditory  perceptions) 
or  olfactory  or  gustatory  hallucinations  or  cutaneous  paresthesiae  (the  feeling 
of  a  wind  blowing  on  some  part  of  the  body  is  quite  common)  and  pains  or 
visceral  paresthesiae,  especially  epigastric.  Vertigo  is  a  common  immediate 
aura;  or  the  immediate  aura  may  be  motor  and  consist  in  twitching  of  a  group 
of  muscles,  (Jacksonian  epilepsy),  or  in  more  complicated  automatic  move- 
ments of  the  body,  or  in  hiccough,  sneezing,  yawning  or  swallowing.  Vaso- 
motor disturbances,  flushing  or  pallor  with  secondary  paresthesiae,  are  not  un- 
common immediate  aurae.  Usually  the  aura  is  always  the  same  in  the  same  in- 
dividual ;  rarely  it  varies.  In  rare  cases  the  aura  may  not  be  followed  by  an 
attack  and  in  still  rarer  and  always  doubtful  cases  it  may  be  the  only  symptom 
of  epilepsy. 


Signifi- 
cance 


411 

Jacksonian 
epilepsv 
(587-8, 
602) 


422 

The  pro- 
dromata 
of  apo- 
plexy 
(504, 
1063-6) 


423 

Tabetic 
or  vis- 
ceral 
crises 
(661) 


A  clonic  spasm  of  one  or  more  muscles  in  one  side  of  the  face  or  in  one  arm  or  leg,      Local 
which  may  remain  local,  but  usually  rather  rapidly  extends  to  other  muscles  of      cortical 
the  same  side  of  face,  or  of  the  arm  or  leg  in  wliich  it  commenced.     It  then  may      lesion 
extend  to  an  adjacent  extremity  in  the  same  order  in  which  the  cortical  centers      (587-8, 
are  placed :     thus  from  the  face  to  the  arm  and  then  to  the  leg,  from  the  leg  to      602) 
the  arm  and  then  to  the  face,  from  the  arm  to  the  leg  and  face  nearly  or  quite  (Figs.  15- 
simultaneously,  but  never  from  the  face  to  the  leg, or  vice  versa,  without  involving      16) 
the  arm.     When  the  spasm  has  extended  over  the  whole  half  of  the  body  it  may 
remain  so  or  may  pass  across  and  involve  the  other  side.     As  long  as  the  spasm 
is  local  or  limited  to  one-half  of  the  body  consciousness  may  or  may  not  be  lost, 
but  when  the  spasm  involves  both  sides  of  the  body  consciousness  is  always  lost. 

in  many  cases  of  apoplexy,  especially  in  cases  of  cerebral  thrombosis,  the  apoplectic      Apo- 
attack  is  preceded  by  a  number  of  more  or  less  definite  and  characteristic  symp-      plexy 
toms   which   may   be  remote,   preceding   the  attack  by  months  or  years;  or  im-      (504, 
mediate,  occurring  immediately  before  the  attack.     These  prodromata  are  both      1063-6) 
general,  such  as  headache,  vertigo,  drowsiness  and  stupor,  irritabihty,   forget- 
fulness,  hypochondriacal  feelings,  ringing  in  the  ears,  flashes  before  the  eyes, 
etc. ;  and  local,  such  as  temporary  attacks  of  aphasia,  diplopia,  achromatopsia, 
dysarthria,  temporary  paralysis  of  arm  or  paresthesiae.     None  of  these  symp- 
toms is  so  characteristic  that  an  attack  of  apoplexy  can  be  confidently  predicted 
from  its  presence.     The  most  constant  prodromal  symptom  of  apoplexy  (except 
of  embolism)  is  high  arterial  tension. 

Paroxysmal  attacks  of  pain  in,  and  functional  disturbances  of,  some  viscera,  occur- Xabes 
ring  in  the  course  of  locomotor  ataxia.     These  attacks  recur  after  irregular  in-  (661) 
ter\'als,  persist  during  an  hour,  or  a  day  or  two,  and  are  analogous  to  the  par-  (Fig. 
oxysmally  occurring  lightning-like  pains  in  the  legs.     "Gastric  crises"  are  the  27) 
most  frequent  and  consist  in  severe  pain  in  the  epigastrium  together  wth  uncon- 
trollable vomiting  and  retching.     At  times  attacks  of  gastric  pain  or  of  vomiting 
occur  separately.     "Hepatic  crises"  resemble  gallstone  colic,  even  being  accom- 
panied by  slight  jaundice  at  times.       "Laryngeal  crises"  consist  in  attacks  of 
coughing  and  dyspnoea.     "Laryngeal  vertigo"   (Ictus  laryngeus)   consists  in  a 
sensation  of  tickling  and  burning  in  the  larynx,  a  stridulous  inspiration  vrith  a 
feeling  of  suffocation  and  a  falling  to  the  ground  unconscious  for  a  few  minutes. 
"Pharyngeal  crises"  consist  in  repeated  acts  of  noisy  swallowing.  "Renal  crises" 
resemble  attacks  of  renal  colic.     "Vesical   crises"    consist   in    pain  in  region  pf 
bladder  and  prostate,  and  constant  desire  to  urinate.     "Uretltral  crises"  consist 
in  attacks  of  pain  in  urethra  and  desire  to  urinate.     "Rectal  crises"  consist  in 
attacks  of  pain  in  the  rectum  and  tenesmus.     "Vulva-vaginal  crises"  consist  in 
attacks  of  pain  in  vagina.     "Clitoridean  crises"  consist  of  attacks  of  pain  in  vulva 
with  sexual  desire  and  discharge  of  mucus.     "Anginal  crises"  resemble  angina 
pectoris.     Occasionally  "crises"  of  several  kinds  occur  simultaneously. 


121 


SYNDROMES  AND  SPECIAL  SYMPTOMS  OF  DISEASE  (Continued) 

Syndrome  Definition  Significance 

424  A  combination  of  several  or  all  of  the  following  symptoms  :  dysarthria  or  anarthria  ~i 
Bulbar  (283-4),  dysphagia  (285),  drooling  of  saliva  from  mouth,  propulsive  speech, 

symp-  and  puffing  of  lips.     Paralysis  of  the  7th,  9th,  10th,  11th,  and  12th,  and  at  times 

toms  of  other  cranial  nerves.     Spastic  paraplegia  or  hemiplegia  of  extremities.     Sen- 

(546)  sory  paralyses  and  ataxia.     Respiratory  difficulty,  and  in  severe  cases  rapid,  ir- 

regular pulse  and  Cheyne-Stokes'  respiration. 

425  Long  pauses  in  the  respiration.  After  a  pause  the  respiration  commences  slow 
Chevne-  and  deep  and  rapidly  becomes  quick  and  superficial  and  as  rapidly  becomes  slow 
Stokes'  and  deep  again  and  terminates  in  another  long  pause  (lasting  from  five  to  sixty 

respira-  seconds,  or  more)  and  so  on ;  each  cycle  being  completed  in  a  few  minutes.  A 
tion  somewhat  similar  respiratory  disturbance  wliich  is  called  Biot's  respiration  con- 

(728)  sists    of    frequent    pauses  in  the  respiratory  act,  lasting  many  seconds.     Biot's 

respiration  occurs  in  Bright's  disease,  etc.,  but  has  no  particular  significance  in 

nervous  diagnosis. 


Lesion 
or  dis- 
order 
of 

med- 
ulla 
(546). 
(  Figs. 
21-2) 


426  Slow   pulse   with   long  arrests    (one-half   to   one 

Stokes-Adams'  phenom-  minute  or  more)  during  which  the  patient  be- 

enon  comes  pale,  unconscious  and  may  show  a  more 

(582,   1060)  or  less  pronounced  convulsion. 


Lesion  of  bundle  of 
His  in  the  heart, 
or  irritation  of  the 
pneumogastric  nerve. 


427 

Babinski  and  Nageotte's 
bulbar  syndrome   (1268) 


428 

Ponto-cerebellar  angle 
syndrome  (1377) 


429 

Millard-Gubler's 
syndrome   ( 1292) 

430 

Weber's  syndrome  (1293) 

431 

Benedykt's  syndrome 
(1293,  1341) 


Paralysis  of  the  tongue,  diaphragm  and  larynx    Lesion  of  medulla. 
with  ataxia  of  the  homolateral   side;  analgesia         (Figs.  21-3) 
and  thermic  anesthesia  with  motor  paralysis  of 
arm  and  leg  of  the  contralateral  side,  myosis 
and  pseudo-ptosis,  dysphagia  and  dysarthria. 


Homolateral  deafness  and  contralateral  analgesia 
and  thermic  anesthesia  with  preservation  of 
tactile  sensibility,  nystagmus,  weakness  of 
conjugate  deviation  of  the  eyes  towards  the 
side  of  the  lesion,  anesthesia  and  abolition  of 
reflexes  in  the  distribution  of  the  trigeminus 
on  side  of  lesion,  adiadocokinesia  on  the  same 
side,  optic  neuritis,  cerebellar  ataxia  and  occi- 
pital pains,  all  more  marked  on  side  of  le.sion. 

Homolateral  facial  paralysis  with  conttralateral 
paralysis  of  arm  and  leg. 


Lesion  at  ponto- 
cerebellar angle. 
(Fig.  20) 


Lesion  of  pons. 
(Fig.  20) 


Homolateral   oculo-motor   paralysis   with   contra-    Legion  of  crus 
lateral  hemiplegia.  cerebri. 

Hbmolateral     oculo-motor      paralysis    associated    Lesion    of    red    nucleus 
with  a  tremor  of  the  contralateral  arm  and  leg.    ^    or     of     rubro-spinal 

tract. 


432 
Brown-Sequard's 

paralysis  or 

spinal 

hemiplegia 

f509,  844, 

982) 

433 

Spinal  epilepsv 
(fiO-1  and  520) 

4.34 

Bell's  phenomenon 


Below  the  point   of   lesion  there  are  motor  paralysis,  exaggerated   ten-  Uni- 

don  reflexes,  Babinski  reflex,  elevation  of  temperature,  vaso-motor  lateral 

disturbances,  and  at  times  more  or  less  hyperalgesia,  ataxia,  and  loss  spinal 

of  deep  sensibility  on  the  homolateral  side,  together  with  analgesia,  lesion, 

thermic  anesthesia,  apallesthesia  (353)  and  more  or  less  tactile  anes-  (Figs, 

thesia,  on  the  contralateral  side.     The  anesthesia  is  bounded  above  24-6) 
by    a    narrow    zone   of    hyperesthesia  or  hyperalgesia.     Brown-Se- 
quard's  paralysis  is  more  often  atypical  than  typical. 


Violent  and  continued  tremor  of  the  leg  after  it 
has  been  struck  or  .shaken. 

A  turning  upward  of  the  eyeballs  when  an  at- 
tempt is  made  to  close  the  eyelids  in  peripheral 
facial  paralysis. 

122 


Groat  Iv  exaggerated 
tendon  reflexes. 

Facial  paralysis 
(peripheral). 


SYNDROMES  AND  SPECIAL  SYMPTOMS  OF  DISEASE   (Continued) 


Syndrome 

435 
Stri'impeH's 

tibialis 

phenomenon 

436 

Babinski's  asso- 
ciated move- 
ments of 
trunk  and 
thigh 


Definition 


Significance 


When  a  patient,  wath  spastic  paralysis  of  a  leg,  lying  on  his  back,  attempts 
to  flex  the  paralysed  leg  at  the  knee  against  light  resistance,  a  dorsal 
flexion  of  the  foot  also  occurs.  Strimipell  has  found  similar  phenom- 
ena in  the  radial  and  pronator  groups  of  muscles  in  the  forearm. 

When  a  patient  with  spastic  paralysis  of  one  leg,  lying  on  a  hard  surface 
without  a  pillow,  with  legs  slightly  abducted  and  hands  folded  across 
chest,  attempts  to  raise  the  body  to  a  sitting  posture,  the  paralysed  leg 
is  involuntarily  raised  from  its  support  while  the  normal  leg  lies  at  rest. 
This  movement  does  not  occur  in  hysterical  paralysis. 


Lesion 
ot  the 
pyra- 
midal 
tract. 
(Fig.s. 
24-6) 


437 
Argyll-Robertson 

pupillary  reflex 

(891) 

438 

l<.omberg's  symp- 
tom (static 
ataxia) 

439 

Riernacki's  sign 

440 

Trousseau's   sign 

441 
Chvostek's  sign 

442 
Erb's  sign 


Loss  of  the  pupillary  reflex  to  light,  while  the  reflex  persists  with 
efforts  of  accommodation  and  the  consequent  convergence  and 
parallelism  of  eyeball   (332.) 


A  wavering,  staggering  and  even  falling  when  attempting  to  stand 
still  with  eyes  shut  and  with  the  feet  in  contact,  either  laterally 
or  the  one  before  the  other  (42.) 


A  loss  of  the  normal  sensitiveness  to  pressure  of  the  ulnar  nerve 
behind  the  elbow. 

Pressure  on  the  nerve  trunks  of  the  extremities  causes  a  tetanic 
spasm  of  the  muscles  supplied  by  them. 

The  facial  nerve  shows  extreme  irritability  to  percussion  or  pres- 
sure. 

Muscles  and  nerves  are  unusually  excitable  both  to  galvanism  and 
to  faradism. 


Tabes, 

paresis 
and 

svphilis 
"  (66n. 
Cerebellar 
disease 
(647). 


Tetany 
(614). 


443 
Ouinquand's  sign 


444 

Erb'-;  paralvsis. 
Combined 
shoulder  and  arm 
paralysis  (490) 


445 
Klumpke's 

paralvsis 

(490) 


446 

Brud/inski's 
nerk  sign 
474 
Brudzinski'e  leg  eign 


Patient  spreads  his  fingers  and  presses  their  tips  against  the 
palm  of  the  observer's  hand  which  is  held  vertically. 
After  a  few  seconds  a  series  of  slight  shocks  are  felt  as  if 
the  phalanges  of  each  finger  were  knocking  together. 

A  paralysis  of  the  deltoid,  biceps,  brachialis  anticus  and  supi- 
nators, long  and  short.  In  some  cases  the  supra-and  infra- 
spinatus muscles  are  also  paralyzed,  and  to  a  less  extent  the 
extensors  of  the  wrist  and  fingers.  Anesthesia  of  outer  as- 
pect of  forearm  and  hand  is  occasionally  present.  Para- 
lysis of  5th  and  6th  cervical  nerve  roots. 

A  paralysis  of  the  small  muscles  of  the  hand  and  fingers. 
There  is  anesthesia  of  ulnar  side  of  forearm  and  hand.  In 
some  cases  the  muscles  of  the  forearm,  except  the  supinator 
longus,  are  also  paralyzed,  and  the  eye  on  the  same  side  ex- 
hibits miosis  retraction  of  the  bulb  and  narrowing  of  the 
eyelid  opening.  Paralysis  of  nerves  arising  from  the  7th 
and  8th  cervical  and  1st  dorsal  nerve  roots. 

When  the  arms  and  legs  are  flexed  fully  on  the  trunk  and  the 
head  is  passively  bent  forward  the  patient  shows  signs  of 
pain. 

When  one  leg  is  passively  fully  flexed  on  the  trunk  the  other 
leg  is  drawn  up  by  the  patient  into  a  similar  position. 


Chronic 
alcohol- 
ism. 


Lesion  of 
the  brachial 
plexus. 
Erb's  paral- 
ysis may  be 
due  to 
injury  at 
birth" 
(obstetric 
paralysis.) 


).   Meningitis. 


123 


SYNDROMES  AND  SPECIAL  SYMPTOMS  OF  DISEASE  (Concluded) 


Syndrome 
448 
Crasset  and  Grauiael's 

phenomenon 


Definition  Significance 

Inability  of  a  patient  when  lying  on  his  back  to  raise  both  legs    Organic 
simultaneously  although  he  is  able  to  raise  either  leg  sepa-    hemiplegia 


rately. 


449 

Avellis' 
syndrome 

450 

Schmidt's 
syndrome 

451 

Korsakoff's 
psychosis 

452 

Bristowe's 
syndrome 

453 
Brun's 

syndrome 
454 
Fovi  lie's 

syndrome 
455 
Horner's 

syndrome 

456 

Schiiller's 
side-gait 


Recurrens   paralysis   of   one   side  with  paralysis  of  the  uvula 
of  the  same  side. 

Same   as   Avellis,    and   also   paralysis   of    the   trapezius  and 
sterno-cleido-mastoid  muscles  of  the  same  side. 


Retroactive  amnesia   (769). 
of  time  and  space. 


Failure  to  appreciate  relations 


Progressive  hemiplegia  with  vague  hemiplegic  symptoms  on 
the  other  side.  Drowsiness  increasing  to  coma,  dysphagia 
and  dysarthria,  hut  no  other  implication  of  the  cranial 
nerves. 

Vertigo  associated  with  movements  and  change  of  pxjsition 
of  head. 

I'aralysis  of  face  and  of  oculo-rotary  power  towards  the  same 
side  and  of  arm  and  leg  of  the  opposite  side. 

Miosis,  ptosis,  enophthalmos  and  anhydrosis. 


The    patient    when    stepping    laterally    along    a  straight  line 

walks  badly  in  both  directions. 
The  patient  when  stepping  laterally  along  a  straight  line  walks 

toward  the  f>aralysed  side  and  badly  towards  the  healthy 

side. 


(incom- 
plete) 

Lesion  of 
nuclei  in 
the  medulla 
(706) 


Alcoholism 
(1102) 

Lesion  of 
the  corpus 

callosum 
(1300) 

Intra- 
ventricular 
lesion  (1008) 
Lesion  of 
tegmentum 
of  pons  (1292) 
Paralysis  of 
cervical 
sympathetic 
ganglion  (1 191) 
Hysterical 
hemiplegia  (796) 
Organic 
hemiplegia 
(797) 


ANATOMICAL  TERMS 


460 
Brain  stem 

461 

Cortico-spinal 
or  upper 
motor  neurons 

462 
Spino-muscular 

or  lower 

motor  neurons 

463 

Central  sensory 

or  upper 

sensory  neurons 

464 

Peripheral  sensory 

or  lower 

sensory  neurons. 

465 

Cilio-spinal  center 
(335.  1191-2) 


Comprises  the  medulla  oblongata,  pons  VaroHi  and  crura  cerebri.     (Figs.  18-23.) 

Motor  cerebral  cortex,  corona  radiata,  internal  capsule,  pyramidal  tracts  at  base 
of  brain,  motor  decussation  and  crossed  and  direct  pyramidal  tracts  in  spinal 
cord.     (Figs.  15-26.) 

Motorial  end  plates,  peripheral  nerves,  anterior  nerve  roots,  nerve  cells  in  the  an- 
terior horns  of  spinal  cord  and  the  motor  nuclei  in  the  brain  stem.  (Figs.  19, 
26.) 

Sensory  cerebral  cortex,  corona  radiata,  internal  capsule,  cerebellum  and  its 
jjcduncles,  lemniscus  and  sensory  decussation,  nuclei  of  columns  of  Goll  and 
Burdach,  antero-lateral  ascending  (Gower's)  tract,  direct  cerebellar  (Flech- 
sig's)  tract  and  column  of  Clark.     (Figs.  15-26.) 

Sensory  end  organs,  peripheral  nerves,  posterior  nerve  roots,  spinal  ganglia, 
posterior  horns  and  columns  of  Goll  and  Burdach  in  the  spinal  cord  and  nuclei 
of  columns  of  Goll  and  Burdach.     (Figs.  22-6.) 

Situated  in  the  lateral  horn  of  gray  matter  in  the  last  cervical  and  first  dorsal 
segment  of  the  spinal  cord  and  is  connected  with  a  higher  center  in  the  medulla. 
Destructive  lesions  of  this  center  and  its  nerve  roots  cause  (1st)  a  paralytic 
miosis,  (2d)  a  narrovring  of  the  eyelid  opening,  (3d)  an  enophthalmos;  while 
irritative  lesions  (rare)  of  this  center  and  its  nerve  roots  cause  (1st)  a  spas- 
modic mydriasis,  (2d)  an  exophthalmos  (Homer's  Sydrome — 455). 

124 


PART  II 

Differential  Diagnosis 

A  Clinical  Diagnostic  Analysis  of  the  Symptoms 

OBTAINED  FROM  THE  EXAMINATION  OF  PATIENTS 


125 


Introduction  to  the  Diagnostic  Cliarts 

DIRECTIONS   FOR  THEIR  USE. 

In  using  this  book  for  diagnostic  purjwses  the  student,  or  practitioner,  having  made  a  com- 
plete examination  of  the  patient  according  to  the  scheme  presented  in  chart  I,  should  make  note 
of  the  more  important  symptoms.  Then,  selecting  any  one  of  these  symptoms,  he  should  turn 
to  the  table  of  contents  and  see  which  chart  treats  of  the  disorders  which  include  this  symptom. 
Finally,  turning  to  the  commencement  of  the  chart  indicated,  he  should  apply  one  test  after 
another  until  he  reaches  the  diagnosis. 

At  the  left  margin  of  each  chart  is  placed  the  symptom  to  be  analyzed;  on  the  right  margin 
are  placed  all  the  possible  diseases  in  which  this  symptom  can  occur.  Proceeding  from  left 
to  right,  in  each  column  a  number  of  alternatives  are  offered,  and  by  selecting  the  one  appro- 
priate to  the  case  the  diagnostician  proceeds  from  one  column  to  the  next,  until  he  reaches  the 
correct  diagnosis.  In  the  column  immediately  preceding  the  diagnosis  is  an  abstract  of  most 
of  the  svmptoms  which  may  occur  at  different  stages  of  the  disease.  The  great  majority,  but 
not  necessarily  all,  of  the  symptoms  given  in  the  abstract  should  be  present  in  the  history  or 
found  in  the  examination  of  the  case,  if  the  diagnosis  be  correct. 

A  few  practical  examples  will  illustrate  the  method  much  better  than  a  long  general  descrip- 
tion. Let  us,  then,  consider  a  few  cases  as  they  occur  in  actual  practice.  Only  the  essential 
symptoms  are  noted. 

Case  I.  Male,  aet.  51. — He  smoked  and  chewed  tobacco  and  drank  to  excess  for  years. 
About  two  months  ago  he  began  to  have  pains  at  various  points  in  both  legs.  His  legs  became 
slowly  weaker  and  his  flesh  became  tender,  but  he  is  able  to  walk  a  mile.  Organic  reflexes 
normal.  Feet  cold,  and  the  legs  have  lately  grown  smaller.  On  physical  examination  the 
muscles  of  the  lower  legs,  and  less  so  those  of  the  thighs  are  weak,  tender  and  somewhat  atro- 
phied. The  legs,  and  especially  the  feet  show  slight  anesthesia,  marked  anaigesia  and  well 
marked  retardation  of  the  conduction  of  pain.  Achilles  reflex  absent.  A  slight  knee-jerk  can 
be  obtained  with  difficulty.     In  walking  toes  drop  a  little  and  the  knees  are  raised  abnormally  high. 

Important  symptoms:  Paralysis  (weakness!),  High -stepping  Gait,  Anesthesia  and 
Pain. 

The  chief  symptom  in  this  case  is  weakness,  and  we,  therefore,  turn  to  chart  X,  which  dis- 
cusses "diseases  causing  motor  paralysis."  The  paresis  in  this  case  is  continuous  and  the  reflex 
acts  are  diminished  or  absent.  We,  therefore,  have  to  do  with  a  flaccid  paralysis  and  turn  to 
chart  Xa.  The  presence  of  muscular  atrophy  following  the  paralysis,  together  with  the  absence 
of  any  apparent  hypertrophy,  guides  us  in  the  second  column  away  from  the  functional  diseases 
and  the  muscular  dystrophies  and  to  the  degenerative  atrophies ;  while  the  normal  organic 
refle.xes  guide  us  in  the  third  column  away  from  the  spinal  cord,  and  to  the  peripheral  nerve, 
diseases.  The  presence  of  anesthesia,  pains,  muscle  tenderness  and  other  sensory  symptoms 
guides  us  in  the  fourth  column  to  the  class  of  neuritis  of  the  spinal  nerves.  In  the  fifth  column 
the  fact  that  there  are  many  spinal  nerves  affected  guides  us  to  the  diagnosis:  Multiple  Neuritis, 
which  the  history  of  alcoholic  abuse  confirms. 

We  can  approach  this  case  in  another  way  by  considering  his  abnormal  walk.  In  the  table 
of  contents  we  find  that  disorders  of  gait  are  treated  in  chart  XIII  and  indeed  in  chart  XIIIc. 
The  walk  in  this  case  is  evidently  "paralytic  and  flaccid,"  the  tendon  refle.xes  being  diminished. 
Furthermore  it  is  a  high-stepping  gait.  A  comparison  of  the  three  possible  abstracts  with  the 
symptoms  of  our  case  makes  it  evident  that  the  case  is  one  of  Multiple  Neuritis. 

We  can  trace  the  case  also  by  means  of  the  anesthesia  and  analgesia :  symptoms  which  are 
discussed  in  chart  XlVa.  The  tendon  reflexes  being  diminished  and  the  organic  reflexes  normal 
in  this  case,  we  are  led  to  three  abstracts,  only  one  of  which  fits  our  case,  and  thus  the  diagnosis 
of  Multiple  Neuritis  is  again  confirmed.  Finally  we  may  take  up  the  initial  symptom  in  the 
case:  pain  in  the  legs.  Pain  is  discussed  in  chart  XV  and  pain  in  the  extremities  in  chart  XVc. 
In  our  case  the  pain  is  bilateral  and  is  associated  with  anesthesia;  so  that  we  are  again  brought 
to  three  abstracts,  of  which  the  one  of  Multiple  Neuritis  most  nearly  fits  our  case. 

127 


Case  II.  Female,  aet.  23. — Ten  years  ago  she  and  her  brother  had  simultaneously  an 
attack  of  headache,  backache  and  fever.  Her  brother  died  and  she  recovered  with  a  paralysis 
of  both  legs,  which  has  since  improved,  rapidly  at  first,  then  more  slowly.  Her  legs  are  still 
somewhat  weak,  especially  the  left  one,  but  she  can  walk  fairly  well.  No  sensory  disturbances, 
organic  reflexes  normal.  On  physical  examination  there  is  a  decided  weakness,  slight  atrophy 
and  slight  shortening  of  left  leg.  Knee-jerks  are  absent  in  both  legs.  No  objective  sensorj' 
abnormalities.  !^i?i''  '        ' 

Important  symptom :     Par.^lvsis. 

In  the  analysis  of  this  case  we  follow  the  same  path  traced  in  case  I  until  we  reach  column 
four  in  chart  Xa.  In  this  case  there  are  no  sensory  symptoms,  the  paralysis  involves  neither 
the  cranial  nor  the  extensor  nerves  exclusively,  and  is  acute  in  its  origin ;  so  that  the  diagnosis 
must  be  Acute  Anterior  Poliomyelitis. 

Case  III.  Male,  aet.  48. — Had  a  chancre  followed  by  a  cutaneous  rash  twenty-two  years 
ago.  During  the  past  ten  years  has  had  "lightning  pains"  in  legs  and  a  girdle  sensation,  also 
gastric,  vesical  and  urethral  crises.  During  the  past  six  months,  his  walking  has  become  diffi- 
cult and  awkward  and  is  much  worse,  practically  impossible,  in  the  dark.  Organic  reflexes 
normal,  except  for  some  delay  in  micturition.  On  physical  examination  there  is  no  loss  of 
muscular  power,  but  all  movements  of  legs  are  awkward,  violent  and  excessive.  There  are 
marked  ataxia,  anesthesia  in  areas  and  well  marked  retardation  of  conduction  of  pain  from 
feet.  Complete  absence  of  knee-jerk.  Argyll-Robertson  pupillary  reflex,  Romberg's  symptom 
and  loss  of  muscle  sense  in  legs.  Lumbar  puncture  gave  fluid  showing  the  pressure  of  globulin 
and  lymphocytosis  and  a  positive  Wassermann.  In  walking  the  patient  does  not  stagger,  but 
flings  feet  out  widely. 

Important  symptoms:  Ataxia,  Ataxic  Gait,  Anesthesia.  Pain,  Abdominal  Crises, 
and  Lymphocytosis  in  Cerebro-spinal  Fluid. 

In  tliis  case  there  is  no  loss  of  motor-power  but  well  marked  ataxia  in  legs.  From  the 
table  of  contents  we  learn  that  diseases  cau.sing  perversion  of  motion,  including  ataxia,  are  treated 
in  chart  Xlla,  to  which  we  turn.  As  the  patient  does  not  stagger  in  walking  and  the  move- 
ments of  the  legs  are  ataxic,  not  only  in  walking,  but  also  in  other  movements,  it  is  certain  that 
the  case  is  one  of  "motor  ataxia."  The  ataxia  is  bilateral  and  the  knee-jerks  are  absent;  so 
that  it  is  evident  that  we  have  to  do  with  tabes  or  multiple  neuritis  (pseudo-tabes).  We  differ- 
entiate these  two  diseases  by  comparing  the  abstracts  of  their  symptoms.  As  in  this  case  there 
are  no  muscular  weakness,  atrophy  and  tenderness,  it  is  plain  that  the  diagnosis  is  Tabes. 

We  may  also  reach  a  diagnosis  in  this  case  by  studying  the  patient's  walk  with  the  aid  of 
chart  XIIIc.  The  gait  is  ataxic,  rather  incoordinated  than  staggering,  the  knee-jerks  are 
abolished  and  there  is  .\rgyll-Robertson  phenomenon ;  so  that  the  diagnosis  of  Tabes  is  con- 
firmed. Furthermore  ve  may  trace  the  case  by  the  symptom  of  anesthesia  with  the  aid  of 
chart  XlVa.  The  terdo  i  reflexes  are  abolished.  The  organic  reflexes  are  not  much  disordered, 
but  they  are  slightly.  There  is  no  motor  paralysis  and  thus  we  are  led  again  to  Tabes.  If 
we  consider  the  symptom  named  "Argyll-Robertson  phenomenon,"  which  is  present  in  tliis 
case,  we  shall  find  it  discussed  in  chart  XI Vd  and  here  again  we  are  led  directly  to  Tabes.  If 
we  consider  the  pains  in  the  legs  or  the  girdle  sensations  about  the  body  or  the  abdominal  crises, 
we  find  them  discussed  in  chart  XV  and  in  either  case  are  led  to  Tabes.  If  we  consider  the 
results  of  the  examination  of  the  cerebro-spinal  fluid  with  the  aid  of  chart  XIX,  we  find  the 
butyric  acid  test  positive,  the  existence  of  lymphocytosis,  a  positive  Wassermann,  a  clear  fluid 
and  ataxia,  and  thus  the  diagnosis  of  Tabes  is  again   confirmed. 


Case  IV.  Female,  aet  19. — Patient's  father  and  mother  were  first  cousins.  They  had 
eight  children,  of  whom  three  died  in  infancy  and  four  are  healthy.  Child  learned  to  walk 
late  and  with  difficulty,  frequently  stumbled  and  fell.  Was  backward  at  school  and  when  she 
was  nine  years  old  it  was  evident  to  all  that  she  was  not  normal.  Patient's  movements  became 
gradually  and  steadily  more  awkward.  Now  she  cannot  walk  without  aid.  General  movements 
are  slightly  ataxic  and  simulate  somewhat  tremor.  Movements  of  the  legs  are  more  ataxic  and 
weaker  than  those  of  the  arms.  Her  walk  is  extremely  ataxic  and  staggering.  No  knee-jerks, 
Rabinski  present.     Organic  reflexes  normal.     Internal  strabismus.     No  loss  of  mu.scle  sense. 

Important  symptoms:     Ataxia  and  Ataxic  Gait. 

128 


The  most  characteristic  symptom  in  this  case  is  ataxia  and  so,  as  in  case  III,  we  turn  to 
chart  Xlla.  In  this  case,  the  ataxia  is  mainly  on  \v;ilkiiig  and  thtre  are  no  motor  paralysis  and 
no  loss  of  muscle  sense.  We  are,  therefore,  brought  to  the  alternative  as  to  whether  the  disease 
occurs  in  an  adult  or  a  child.  This  case  doubtless  dates  from  early  childhood.  There  are  no 
similar  cases  among  her  brothers  and  sisters,  but  she  comes  certainly  from  a  tainted  family. 
She  has  no  nystagmus,  but  has  strabismus.  As  this  case  began  before  puberty  and  has  no  knee- 
jerks  it  is  doubtless  a  case  of  Friedreich's  Ataxia.  The  strabismus  points  to  Marie's  hereditary 
cerebellar  disease  and  indeed  these  two  diseases  are  so  closely  related  that  there  is  some  ques- 
tion as  to  whether  they  are  separate  entities. 

We  may  approach  this  case  from  a  different  angle.  The  chief  symptom  is  difficulty  in  walk- 
ing. We  turn,  therefore,  to  chart  XIIc  and  note  that  the  walking  is  ataxic.  The  staggering 
gait  which  is  permanent,  the  bad  heredity,  the  absence  of  knee-jerk  and  the  commencement 
of  the  disease  in  infancy  confirms  the  diagnosis  of  Friedreich's  Ataxia.  It  may  be  noted  in 
passing  that  this  case  does  not  show  a  distinct  tremor,  or  nystagmus,  or  the  blurred  speech  which 
symptoms  are  often  present  in  this  disease. 

Case  V.  Male,  aet.  62. — His  disease  commenced  with  difficulty  in  speaking  and  swallow- 
ing about  a  year  ago,  and  has  slowly  and  steadily  progressed.  His  speech  has  become  so  bad 
that  it  is  unintelligible  and  he  has  the  greatest  difficulty  in  swallowing,  and  chokes  over  his 
food.  There  is  constant  drooling  of  saliva  from  his  mouth.  Cannot  protrude  his  tongue  beyond 
his  teeth,  cannot  raise  his  arms  because  of  weakness  of  muscles  about  the  shoulders.  His  legs 
are  somewhat  weak.  Fibrillary  contractions  and  great  atrophy  of  muscles  of  tongue  and  of 
shoulder  girdle  (deltoid,  pectorals,  etc.).  Muscles  of  hands  are  not  involved.  Absence  of 
tendon  reflexes  in  arms.  Knee-jerks  lively,  ankle-clonus  and  Babinski  are  present.  There 
are   no    sensory   disturbancesL 

Important   symptoms :     Paralysis,   Fibrillary    Contraction    and    Muscular    Atrophy. 

The  principal  symptom  in  this  case  is  a  motor  paralysis.  We  turn,  therefore,  to  chart  X. 
The  paralysis  certainly  is  a  continuous  one  and  of  the  three  alternatives  next  offered  us  we  must 
select  the  third,  inasmuch  as  we  have  a  flaccid  paralysis  with  muscular  atrophy  in  the  head  and 
arms  and  a  mild  spastic  paralysis  in  the  legs.  We  turn,  therefore,  to  cliart  Xc.  In  this  case 
the  cranial  and  spinal  nerves  are  involved,  next  there  are  no  sensory  symptoms,  next  the  disease 
is  chronic,  and  finally  the  lips,  tongue,  larynx  and  pharynx  are  involved:  consequently  the  diag- 
nosis is  Progressive  Bulbar  Paralysis.  But  this  diagno.sis  does  not  explain  the  paralysis  and 
atrophy  of  the  muscles  of  the  shoulder  which  are  supplied  by  spinal  nerves.  We  turn,  there- 
fore, to  the  next  sub-division,  where  spinal  nerves  are  alone  involved,  and  follow  through,  no 
sensory  symptoms  and  through  a  paralysis  involvincr  the  shoulder  girdle  muscles,  and  reach 
the  diagnosis  of  Amyotrophic  Lateral  Sclero'^is.  The  diagnosis  is,  then,  a  combination  of  two 
diseases :  Progressive  Bulbar  Paralysis  and  Amyotrophic  Lateral  Sclerosis,  and  we  find  in  the 
abstracts  of  these  diseases  that  they  often  occur  together  in  combination. 

If  we  consider  the  symptom  "fibrillary  contraction"  with  the  aid  of  chart  Xllb,  it  is  evi- 
dent that  this  is  an  organic  and  not  a  functional  disease,  that  there  is  a  marked  muscular  atrophy 
and  that  there  are  no  sensory  symptoms,  and  thus  the  diagnosis  of  both  Progressive  Bulbar 
Paralysis  and  Amyotrophic  Lateral  Sclerosis  is  confirmed.  Finally  if  we  consider  the  symptom 
"mtiscular  atrophy"  with  the  aid  of  chart  XVITa  we  find  that  the  atrophy  is  considerable  and 
of  a  relatively  rapid  course,  that  there  are  no  muscular  hypertrophy  and  no  sensory  symptoms 
and  thus  we  are  led  again  to  the  same  diagnosis. 


Case  VI.  Male,  aet.  12. — During  the  first  year  of  his  life  the  child  had  great  difficulty  in 
retaining  food.  At  the  end  of  his  first  year  he  began  to  have  convulsions  with  unconscious- 
ness, and,  with  the  exception  of  an  interval  of  two  years,  these  have  continued  up  to  the  present 
time:  the  last  attack  having  occurred  three  weeks  ago.  The  child  has  a  very  small  head  and 
an  idiotic  expression  of  face.  He  apparently  understands  most  of  what  is  said  to  him,  but  he 
can  talk  only  a  very  little  and  only  a  few  words  are  intelligible.  There  are  no  contractions  or 
deformities,  and  he  uses  his  arms  and  legs  well. 

Important   symptoms:     Anarthria   and   Idiocy. 

The  most  striking  symptom  in  this  case  is  that  a  boy  of  twelve  years  can  scarcely  s|>eak 
intelligibly.  Turning  to  the  table  of  contents  we  find  that  disorders  of  speech  are  treated  in 
chart  XIII,  to  which  we  turn.     The  loss  of  speech  in  this  case  is  so  nearly  complete  that  it  can 

129 


be  called  anarthria,  which  is  discussd  in  chart  Xllla.  The  disease  is  evidently  congenital, 
and  the  expression  of  the  face  is  idiotic,  and  reading  and  writing  are  impossible;  so  that  the 
diagnosis  is  Idiocy.  Had  we,  on  the  other  hand,  decided  that  the  child  could  speak,  but  very 
imperfectly  and  unintelligibly  we  should  have  sought  for  the  disease  in  the  same  chart  Xllla, 
under  the  heading  of  dysarthria.  Here  the  congenital  nature  of  the  defect  and  the  absence  of 
cleft  palate,  etc.,  would  have  led  us  directly  to  Imbecility.  In  order  to  trace  the  case  further 
let  us  follow  the  cross  reference  after  idiocy  which  is  1081  and  which  we  find  in  chart  XVIc. 
This  case  on  account  of  his  convulsions  might  be  classed  under  Epileptic  Idiocy  or  on  account 
of  his  small  head  under  Microcephalic  Idiocy,  or  under  both. 


Case  VII.  Female,  aet.  53. — Complains  of  trembling  and  that  she  cannot  execute  any 
movement  quickly,  because  her  arms  and  legs  are  stiff  and  rigid.  When  walking  she  has  a 
decided  tendency  to  pitch  forward.  Feels  warm  at  times  when  the  room  seems  cool  to  others. 
Expressionless  face,  passive  tremor  of  hands.  Propulsion  and  retropulsion  when  walking  or 
standing.  Rigidity  of  arms  and  legs.  Difficulty  in  rising  frotn  a  low  chair.  Knee-jerks  rather 
increased. 

Important  symptoms:     Muscular   Rigidity,  Tremor  and  Abnormal  Walk. 

The  most  characteristic  symptom  in  this  case  is  the  rigidity  of  the  amis  and  legs  which  is 
a  mild  tonic  spasm.  From  the  table  of  contents  we  learn  that  diseases  causing  spasm  are 
treated  in  chart  XI,  to  which  we  turn  and  find  that  general  tonic  spasm  is  discussed  in  chart  Xlb. 
In  this  case  there  is  no  fever  and  of  the  five  sub-divisions  under  this  head,  this  case  clearly  falls 
in  the  second :  "rigidity  which  does  not  prevent  passive  or  voluntary  motions."  Of  the  two 
alternatives  next  offered  it  is  evident  that  we  must  choose  the  second,  in  the  abstract  of  which 
we  find  all  the  symptoms  present  in  our  case.       The  diagnosis    is,    therefore.    Paralysis  Agitans. 

If  we  follow  the  symptom  "tremor,"  we  find  this  treated  in  chart  Xllb.  It  is  a  passive 
tremor  and,  whether  it  be  increased  or  diminished  on  voluntary  movements,  if  it  be  slow,  the 
abstracts  show  that  it  is  a  case  of  Paralysis  Agitans,  because  the  other  abstracts  do  not  fit  this 
case  at  all. 

If  we  consider  the  difficulty  in  walking  in  this  case  we  turn  to  chart  XIIIc.  In  the  three 
great  divisions  offered  this  case  evidently  falls  in  the  third :  "paralytic  and  spastic ;"  and  of 
the  two  sub-divisions  next  offered  we  must  take  "general  rigidity"  which  leads  us  again  to 
the  diagnosis  of  Paralysis  Agitans. 


Case  VIII.  Male,  aet.  59. — During  the  past  34  years  has  had  at  times  attacks  of  asthma. 
During  the  past  four  years  has  been  troubled  by  a  great  many  paro-xysmal  attacks  of  vertigo, 
at  irregular  intervals ;  some  are  slight,  some  are  so  severe  as  to  throw  him  from  a  chair  half  way 
across  the  room  to  the  floor,  where  he  must  lie  for  several  hours,  because  when  he  raises  his  head 
from  the  floor  he  vomits  violently  and  the  dizzim-ss  becomes  worse.  He  often  has  slight  attacks 
of  vertigo,  which  make  him  stagger  when  walking.  During  these  four  years  he  has  been  slowly 
growing  deaf  in  his  left  ear;  the  deafness  being  now  extreme.  He  has  also  had  during  the  same 
time  in  the  same  ear,  a  buzzing  and  a  ringing  which  is  most  intense  just  before  an  attack  of 
vertigo.  He  has  no  paraly.sis  and  no  loss  of  muscle  sense.  Bone  conduction  is  absent.  He 
also  is  much  troubled  by  gastric  flatulence,  to  which  he  attributes  his  vertigo,  but  when  he  takes 
digestive  medicine  and  the  digestive  disturbances  arc  relieved,  the  vertigo  remains  unchanged. 
His  eyes  were  found  to  he  astigmatic  and  proper  glasses  used,  but  no  improvement  in  the  attacks 
of   vertigo   followcfl. 

Three  vears  after  the  above  record  was  made  the  attacks  were  milder  and  less  frequent, 
but  at  that  time  his  left  ear  was  totally  deaf  and  deafness  was  advancing  in  his  right  ear. 

Important  symptoms:     Paroxysmal  Vertico.  Staggering  Walk  and  Deafness. 

In  this  case  the  principal  symptom  is  paroxysmal  attacks  of  vertigo;  diseases  causing  which, 
we  learn,  are  treated  in  chart  XVd.  We  see  from  this  chart  that  vertigo  may  be  caused  by 
digestive  disturbances  and  disease  of  the  eye,  both  of  which  were  present  in  this  case,  but  the 
vertigo  persisted  when  these  abnormal  conditions  were  relieved;  so  that  they  could  hardly  be 
the  cause.  On  the  other  hand,  we  find  that  vertii,'ci  is  asso<-iate(l  with  deafness,  a  prominent 
symptom  in  this  case,  and  in  looking  over  the  abstract  of  this  form  of  vertigo  we  see  that  it 
fits  the  case  exactly ;  so  that  the  diagnosis  is  Meniere's  Disease. 

130 


If  we  consider  another  symptom,  "the  occasional  staggering  in  walking,"  we  find  this  treated 
in  chart  Xlla.  This  patient  has  no  loss  of  muscle  sense  and  no  muscular  paralysis.  He  is 
an  adult  and  his  hearing  is  abnormal  and  thus  we  are  led  again  to  Meniere's  Disease.  Finally 
if  we  trace  the  symptom  "deafness"  with  the  aid  of  chart  XlVe  we  find  that  the  deafness,  at  any 
rate  at  first,  was  unilateral,  that  bone  conduction  is  absent,  that  there  is  no  facial  paralysis  and 
that  severe  paroxysmal  vertigo  and  tinnitus  aurium  are  presei:t ;  thus  confirming  again  the  diag- 
nosis. 

Case  IX.  Female,  aet.  17. — Heredity  good.  Was  well  until  about  three  years  ago  when, 
at  the  time  of  commencing  menstruation,  she  began  to  have  attacks  of  clonic  convulsions  with 
unconsciousness,  which  have  continued  up  to  the  present  time  and  in  which  she  has  occasionally 
bitten  her  tongue.  Has  also  lesser  attacks  of  unconsciousness,  or  very  cloudy  consciousness, 
in  which  she  automatically  prays,  or  says  foolish  things.  Has  no  memory  of  any  of  her  attacks. 
She  has  an  immediate  aura  of  fire  before  her  eyes  and  of  wheels  revolving  in  her  head.  Some 
headache  follows  the  attack.  The  convulsions  occur  only,  and  the  lesser  attacks  mainly,  at 
night.  Physical  examination  is  negative,  urine  normal.  Fundus  of  eye  normal.  Knee-jerks 
equal.     Much  acne  on  face. 

Important  symptoms:     Coma  and  Convulsions. 

The  constant  symptom  in  all  her  attacks  is  unconsciousness,  or  coma,  of  short  duration. 
This  symptom  is  treated  in  chart  XVIa.  There  is  no  history  of  recent  injury,  of  brain  disease, 
of  poisoning,  of  heart  disease,  of  paralysis,  of  kidney  disease  or  of  fever.  Therefore,  we  are 
led  at  once  to  the  diagnosis  of  Epilepsy  or  of  Eclampsia.  The  latter  can  be  excluded  by  the 
frequently  recurring  attacks  at  long  intervals. 

If  we  next  take  the  symptom  of  clonic  convulsion  with  the  aid  of  chart  XIa,  we  find  that 
there  is  no  fever  and  the  convulsion  is  a  universal  one,  and  not  local  at  the  onset.  There  is 
coma  and  there  are  no  symptoms  of  disease  ol  the  brain  or  cord,  or  of  the  kidneys,  heart  or 
blood,  or  of  poisoning  and  thus  we  confirm  the  diagnosis  of  Epilepsy. 

Case  X.  Female,  aet.  34. — Nine  years  ago  one  morning,  her  left  arm,  leg  and  side  of  face 
felt  numb  and  she  could  not  see  things  on  her  left  side  without  turning  her  head.  These  symp- 
toms steadily  increased  during  the  day  and  she  could  not  use  her  leg,  and  especially  her  arm, 
well.  She  could  always  walk,  but  at  first  she  could  walk  only  with  difficulty.  This  difficulty 
in  walking  gradually  passed  away.  She  could  use  her  arm,  but  could  not  use  it  well  for  more 
than  a  year,  and  it  is  not  quite  right  even  at  the  present  time.  The  numbness  of  the  left  side 
and  the  inability  to  see  things  on  her  left  stiU  persist.  On  physical  examination  there  are  found 
anesthesia  and  analgesia  of  the  left  arm  and  leg  and  left  side  of  body  and  face,  (left  hemi- 
anesthesia and  hemianalgesia) ,  also  blindness  in  each  eye  for  all  objects  to  the  left  of  central 
vision  (left  homonymous  hemianopia).  The  left  arm  and  leg  are  a  little  awkward  and  a  trifle 
weak;  strength  of  left  hand  grasp  to  that  of  right  is  as  80  to  105.  Knee-jerks  lively,  perhaps 
stronger  on  left  side :  neither  ankle-clonus  nor  Babinski.     Organic   reflexes   normal. 

Important   symptoms:  Hemianesthesia,   Hemianalgesia  and  Homonymous   Hemianopia. 

The  principal  symptoms  of  this  case  are  hemianesthesia,  hemianalgesia  and  homonymous 
hemianopia.  These  are  sensory  symptoms  and  indeed,  symptoms  of  a  diminution  of  sensation. 
We  turn  to  the  table  of  contents  and  find  that  "diseases  causing  a  diminution  of  sensation" 
are  considered  in  chart  XIV,  which  we  next  consult.  Starting  with  disorders  of  sensation  in 
the  first  column,  we  have  five  alternatives  offered  us  in  the  second  column,  among  which  we 
ought,  without  doubt  in  this  case,  to  select  diminution  of  sensation  and  following  this  division 
we  have  in  the  next  column  three  alternatives,  among  which,  undoubtedly,  we  should  select 
anesthesia  and  analgesia  and  turn  to  chart  XlVa.  In  this  chart  we  have  the  alternatives  of 
the  tendon  reflexes  being  either  absent  or  present.  In  the  above  case  they  are  present.  The 
dilemma  in  the  next  column  is  quickly  decided  because  the  organic  reflexes  are  normal.  The 
history  of  a  motor  paralysis  lasting  a  year  oi  more  and  still  slightly  persisting  directs  us  to 
the  first  alternative  in  the  next  column,  especially  as  there  are  no  hysterical  symptoms  present; 
while  the  unilateral  nature  of  the  symptoms  and  next  the  acute  onset  (one  day)  brings  us  to 
the  diagnosis  of  Cerebral  Hemorrhage  or  Softening. 

To  determine  which  lesion  is  present,  we  follow  the  first  cross  reference.  No.  503-6,  which 
we  find  in  chart  Xb.  In  looking  over  the  abstracts  differentiating  cerebral  hemorrhage,  embol- 
ism and  thrombosis,  our  case,  with  its  relatively  slow  onset,  its  absence  of  any  coma,  its  absence 
of  any  source  for  an  embolism,  is  probably  one  of  cerebral  thrombosis  and  certainly  one  of  cere- 
bral apoplexy. 

131 


The  next  question  is  as  to  the  locality  of  the  softening.  To  ascertain  this  we  turn  to  the 
table  of  contents  and  find  that  "localization  from  symptoms  of  paralysis"  is  discussed  in  chart 
XXII  to  which  we  turn.  The  reflexes  being  present  in  our  case,  we  are  brought  to  the  ques- 
tion :  whether  sensory  or  motor  paralysis  is  dominant.  In  our  case  sensory  paralysis  is  dominant 
and  we  turn  to  chart  XXIIc.  Of  the  first  alternative  offered  us  in  this  chart  we  must  choose 
the  first:  anesthesia  and  analgesia.  In  regard  to  the  next  column,  the  distribution  of  the  anes- 
thesia in  our  case  evidently  falls  into  the  class:  "the  (left)  arm.  leg  and  face  are  anesthetic." 
In  our  case  there  is  no  Jacksonian  epilepsy  and  there  is  hemianopia,  so  that  the  localization  of 
the  softening  is  in  the  posterior  part  of  the  right  internal  capsule.  If  we  now  turn  to  Fig.  17 
we  can  easily  see  how  a  lesion  in  the  posterior  portion  of  the  internal  capsule  can  easily  involve 
the  sensory  fibers  from  one-half  the  body  and  also  the  optic  fibers;  the  continuation  of  the  optic 
tract.  It  is  also  easy  to  understand  that  on  account  of  the  wide-spread  circulatory  disturbances 
in  the  early  stages  of  the  disease,  before  a  collateral  circulation  liad,  to  a  degree,  reestablished 
itself  in  the  periphery  of  the  lesion,  the  motor  fibers  lying  directly  anterior  should  be  involved 
and  a  more  or  less  temporary  hemiplegia  should  occur,  as  was  indeed  the  case.  It  might  seem 
strange  that  deafness  did  not  occur  in  this  case  as  it  is  certain  that  the  auditory  fibers  also  must 
have  been  involved  in  the  lesion,  but  it  is  well  known  that  central  lesions  only  produce  deafness, 
even  unilateral  deafness,  when  the  lesion  is  bilateral  (see  page  S.) 

Thus  we  have  arrived  by  means  of  the  charts  to  the  diagnosis  of  this  case  of  "thrombosis 
of  the  artery  supplying  the  posterior  portion  of  the  internal  capsule  "  but  in  order  to  make  this 
diagnosis  doubly  sure,  let  us  take  another  one  of  the  prominent  svmptoms,  such  as  homonymous 
hemianopia,  and  follow  it  through  the  charts.  This  symptom  is  also  a  diminution  of  sensa- 
tion and  therefore  we  turn  again  to  chart  XIV.  Disregarding  this  time  diminution  of  sensa- 
tion we  follow  "disturbances  of  vision"  and  "limitation  of  field  of  vision"  to  chart  XlVb.  Here 
we  find  homonymous  hemianopia  and  in  the  next  column  there  can  be  no  doubt  that  we  must 
choose  the  path  which  hemianesthesia  indicates  and  by  it  are  led  to  the  diagnosis  of  hemorrhage, 
or  softening,  in  the  posterior  part  of  the  posterior  limb  of  the  contralateral  internal  capsule, 
which  is  the  diagnosis  which  we  had  already  reached  by  another  road. 


132 


CHART  X 

Motor  Paralysis 


DIAGNOSTIC  ANALYSIS  OF  SYMPTOMS. 
Tests 


Symptoms 
Analyzed 


Permanence 
OF  Paralysis 


469 

MOTOR  PAR- 
ALYSIS OR 
PARESIS 
(244) 

After  a  careful 
examination  has 
shown  that 
the  paralysis 
is  a  true  one 
and  is  not 
simulated  by 
any  ankylosis 
or  by  pain  on 
motion. 


470 

CONTINUOUS 
PARALYSIS 


471 

INTER- 
MITTENT 
PARALYSIS. 


Reflexes  in  Paralyzed  Muscles 

The  reflex  acts  in  the  paralysed 
muscles  are  absent  or  decidedly 
diminished. 

472 

FLACCID  PARALYSIS 

Lesions  of  peripheral  motor  neu- 
rons. 

There  are  hypotonia  and  changes 
in  the  electrical  reaction  of  the 
nerves  and  muscles  involved  in 
very  varying  degree  from  simple 
diminution  in  excitability  to 
complete  reaction  of  degenera- 
tion. No  associated  movements 
present. 


The  reflex  acts  in  the  paralysed 
muscles  are  normal  or  exag- 
gerated. 

473 

SPASTIC  PARALYSIS  (251) 

Lesions  of  central  motor  neurons. 

There  is  hypertonia  without  altern- 
ations of  electrical  reaction  of  the 
nerves  and  muscles.  Associated 
movements  (synkineses)  may  be 
present. 

474 

A  combination  of  FLACCID  PAR- 
ALYSIS in  the  upper  part  of  the 
paralyzed  area  and  of  SPASTIC 
PARALYSIS  in  the  lower  part. 

All  the  muscless  of  the  body  and 
head. 

The  muscles  of  one  or  both  legs, 
rarely  of  arms. 

Commencing  in  legs,  extending  to 
arms. 


The  differential  diag- 
nosis of  those  dis- 
seases      in      which 
FLACCID  PAR- 
ALYSIS occurs 
is  set  forth  in 
CHART  Xa. 


The  differential  diag- 
nosis of   those  dis- 
eases in  which 
SPASTIC  PARAL- 
YSIS occurs  is  set 
forth  in 
CHART  Xb. 


Associated  with  a  cervical  rib. 
133 


The    differential    diag- 
nosis of  those  dis- 
eases in  which  there 
is  a  combination  of 
FLACCID  and  of 
SPASTIC  PARAL- 
YSIS, and  of  those 
in  which  INTER- 
MITTENT PARAL- 
YSIS occurs  is  set 
forth  in 
CHART  X  c. 


L 


CHART  Xa 
Flaccid  Paralysis 


Comprising  Numbers  475  to  477  on  left  side  of  Chart 
and  482  to  500  on  right  margin 


y__        -»it€Y 


DJACNOSTir  HYMn-OMS  AND  TB8TS 

J7S  roncpiiilal    or    no-    A  iiiotnr  pnrnlriiii  ot  oiif  (infaolilc  hcmiiilpctal   nr 

llrmlplegio  niiinHl    io    infnucy.       nro  t5>mmun  nml  may  tiiii«k  iho  owiggpraloii  rpfir.\r.i 

or  Diplegin   nr       TJirri-  moy  !)<•  ferpr       hihI  nt  limes  Idiory  or  insanity.    Frwmi-iirly  Hierr  i 

MonopJesia  or  iiri"pl<^lic  «rnip-       wr.brnl  illplmin.  bulbar  •ymprom*   (4241   are  pr( 

(2&4-C,  S>8)    I"'"»  "I  oinn-i.  prpri«iiun«.  flc.  cno  occur  inroliinlaril.v,  bul  no  i 

'Ss'inptomv  "f  irrilalioD    (convulclons,   riciiJily.  '■tc.) 
c  |>iiFiiouniT<I  llinn  nre  symploms  of  paraly«i«. 


Rpmiplrgia.  or 
Moiiuplpsi" 
(3.14.  2r>») 
(Src  a  loo 

Srrlneomyella — 
:i53.  $40-1.) 


4S0 
I-ompMs 

(2.17) 

(Si-r>  nlM 

SyrincnmFeiin   - 

5J3.  840-1.) 


Alm'«t    ntwnyt    In 
adiilii     and     after 
mlil'lle  lifp. 
Smlrtrn     onwl,    or 
n«),  iiSH' 


Illy 


vilh 


(Iff.  Mii.t  1037).  or 
nitli  hearfai'lie  or 
v«rlli:o  niKl  nifnlnl. 
oinfimicm.  Not  in- 
fr«|in-iilly  llio  at- 
tarli  CH.mmi-ne.« 
wtth  a  hernipleKJa 
which  may  or  may 
not  l>e  follriiveil  liy 


DIAGNOSTIC   AKAXYSIS   OF   SYMPTOMS 
ABSTRACT  01.'  SYMPTOMS 
iHilh  silica   (Little's  dlftcnNp)  of  the  body,  or  ul  mie  enlreniilj',  williont  anoMheNia  nad  witli  very  tittle  mu«culnr  ntrophy  (from  disuse).    A  squint  is  common,    llie  \n%  are  often  maiuly  or  alone  parnlyseH,     Iti^dity  nnd  ronlmctiirps 
B.     In  nalkine  there  is  oflMi  «ddii>i(ir  Bp«sm.  "soiMorB  itn\t"  (70S-808t.     Hxlensor  spopm  is  nUo  frrtiucnl.     Epili'^priform  convulsions  are  commun.  both  at  onset  and  dnrini:  Ihi-  wmr^p  of  the  disease.     There  ia  mueli  mental  weaknem 
H  partial  airrsf  of  arowth  of  Uie  panilyscJ  parts.    AthelOKis  anid  post-hem i pi I'pic  chorea  -and  other  motor  disorders  are  common.     Speech  is  commonly  alTe^tcd    (dj-sartliria).     Tlie  organic  reflexes  nr*  not  di^tiirh^. 
■M'nt  nllhoiit  fibrlllnrion  nr  ttfopby.  and  •miomiitic  und  mimilic  aclicns  are  prcservctl.     In  smh  coses  the  eyeballs  will  follow  a  light  o<-  'ihcr  ohjen.  but  cnntiot  be  turned  bj  ai 
ii^'hintary  motions.     Tho  skull  Is  often  sm.iller  on  the  side  of  the  a(recSid  cen'bral  hcmisfdiere.   Tbe  origin  of  the  disease  may  he  pre-noli1  (ciniseiiitall.  nalnl    (bemorrhnge)    and  ponln 

arc  The  dinoise  i^  ofim  the  r-snlt  of  injiu-y  nnd  even  more  frequently  of  syphilis:.  When  not  so.  prodmiunl  sjinptome  (422)  are  usually  present.  Connilt.ions  jic  enmmon.  butb  at  llie  onset  ami  during  (he  course  of  the  dtaense. 
(\hicb  I"  often  inlcffiilttcnt.  Headache  and  menial  Impairment  are  frequent.  The  onset  of  paralysis  is  apoidcctiform.  It  is  usually  motor  only,  is  rather  mild  in  des-ree  uwl  is  usually  Irarwlcnt.  Organic  refleies  normal, 
fercbro-sninal  fluiJ  ofli-n  bloody. 


■  will,  and  lau^liinir.  we(.<pint;.  emotional 
mill    (encephalitis,  encepbalitic  polfomyelliis). 


Sj-n>pli  HIS  ijf  piiriilyhiH  are  more  pronounced  than  these 
nf  irritation  (convulsions  may  occur,  especially  in 
■■oi'tical  leiinns  and  in  hemnrrhaec  into  Ihc  v.'nlfii'lt". 
ill  which  riiiac  lumbar  punclure  may  yield  a  bloody 
lluid.l  The  paraljHis  in  in  part  temporary  and  in  pari 
piTmniient  in  varying  decree.  Slow  improvninenl  with 
aliiioat  perfect  recovery  in  r.ire  cn«c«.  More  or  li'ss 
lir-minnent  mentnl  impainm-nl.  often  very  Blifiht, 
I'liialiy  patients  are  more  emotional  than  previously. 
ICMCBcriiled  reflexes  and  nnkU-<Jonn8  are  present  after 
coinn  ban  I'lniml  up.  RnhiDski  i«  pn«ent  from  (he 
"tnrt-  I'lillinit.  stertorous  renpiralion  Is  common, 
Cbijiie-Sioli'-s  resplratifin  (  42.'>l  and  tracheal  rales  arc 
vi-y  iinfiiiorable  sympionia.  Certain  muHdcs  are  more 
frn|iienTly  an.l  severely  paralysed  in  apoplexy  than 
■Jihet*.     Wirnji'kc'*  nnilitcclion  muwles  (2ri4). 


t  of  both. 


t>u-:  llinr,  in  tJi.'  I<i!  nn'l  1(i-lly  io  ili. 
heniiidcfif  molor  tlirturbiincea  occur  ii 
iiieltc's  predileptioii  miisclcs  (See  2,>4), 

Slmihi-  to  the  above,  but  onset  Is  more 
arlcrial  ten.sion  is  nsuntly  low.  Tlie 
mon  than  in  hcmorrhas''.  hectiunc  (he  1 

'similar  to  the  above,  hut  on^el  may  he 
I      syphilis.     Tlie  arliirinl  Icnsicn  is  iimin 

basilar  artery  or*'  ajore  frequently  nllc 

beinorrliagc  or  embolism. 


I"  i>  'ir  ..f  the  body,  usually  of  motion  only,   rnrel 
(  )n«ei   is  iisiiallv  acenmpiinled  bv  prormiiid 
I        Piihe  is  slow.    Slicbl  vnriatirn>  of  lemi 
I  II  Hilly  high  arterial  tension.    The  d 

irni      rontmcturrs,  causing  (Icsiiin  of  joinu  of  arms  and  extension  of  joint*  of  les.  ar<'  frcfjiient  nnd  of  bad  pronrnosii 
rare  ca-sus.     The  pupils  arc  usually  dilntcti.  sometimfis  uncfiiial  and  always,  in  deep  coma,  inactive.     Certain  muse 


lensalion  only,  somi'lir 
(CfK-.l   of  several  hours 
re  about   Uie  nnrmal  point :  when  the 
iiatly  oeiurs  in  advanced  life.     If  death  dor 


lower  hratinh  of  the  facial  ncr.-e  is  r 

hut  not  alwayi.     In  Itie  coma  there  i^ 

iriation   is  esln'mc  ilio  iirosno'i*  is  liad. 

usually  more 


inch  mon-  completely  and  perninncntly  pan 
>flen  turnini:  of  the  heail.  and  Cinijuciile  ileviu 
TroilroniBta  are  rather  rare  (122).  There  ar 
ipmvement  in  the  paralysis:  first  ii 


ivery  frcm  the  parnlyvis.    Alhelosls  and  other  post- 
'  more  frequcnl'-y  and  severely  paralysed  than  oUiera:  Wcr- 


1  inslantiineous  and  eomn  is  usually  lew  profound  and  sl'orter  and  frequently  is  entirely  absent.  There 
ise  usually  occurs  in  youlli  or  middle  nite,  In  genenil  the  symptom*  are  less  severe  and  lc«s  permancn 
n  is  more  apt  Io  be  cnrticjil.    .Multiple  (mere  than  twol  r"nirrences  are  more  ctimmon  in  embolism  thai 


re  no  pmiTroniata.  There  is  cardiac  disease  or  other  source  for  emboluB.  The 
:  than  in  h'-morrhnge.  Convulsion*,  aphasia  nnd  monoplegia  ore  more  corn- 
in  hemerrlmite. 


>re  k-raiiual.  althniik'ti  still  sud'len  an't  p\ni  al  titnps  ini 
■  hifih.  .\rtjerinl  disease  ia  common.  The  disease  usua 
'd.    Kimultaneous  paralysis  of  many  cortical    functions 


ProdrnmalB  (422)  are  common.  Coma  is  r 
I  ndvanc-d  life,  flulhar  symptoms  are  more  i 
inmon    than    in  hemorrhage.     Multiple  (inin-e 


'  frequently  absent  or  les 
men  Ilinn  in  bomorrbace 
1  two)  recurrences  arc  im 


profound.  Tlierc  is  often  a  history  of 
or  emtiolism,  because  bmncheo  of  Ihc 
re  common  in  thrombosis  thaa  in  either 


Reasory    symptoms 

arf  always  pres- 

ent,   Oriainic  n-- 

flexes     are     nor 

nrndual  onoetKitli- 

mal      nr     only 

out  cnma,  except  as 

sliahlly      dl«or<l- 

a     lermlDal    aymp- 

ered. 

Brain  symptoms.  Steadily  Increas- 
iiie  psychic  disorder,  and  local 
motor  and  sensory  disturbances 
over  Ihc  same  area. 


■bi-s.  \erliro,  vemiliui:  nnd  convulsions.  Ecnernl  or  local,  are 
ion.  Phoked  Msc  I'r  opije  ueurltiM  and  edema  are  usually  prea- 
n  tumor,  mneh  more  rarely  in  al>'»ec«B.  Steadily  increasing 
ia  anil  nn'ri-  or  Ir-s  menial  diillne*9.  Focal  symplnms,  IhiMi 
iKidic  and  iiarelylii',  are  usually  present,  e.*pecially  .Tacksmiian 
psy  r42I,(!0'Jl,  Mjirkedly  increased  tension  of  cerebrospinal 
and  slow  piiUe  in  -lime  of  riinipre-Kinn,  especially  in  tumor. 


li-nds. 

>rien  fever.  A  source  of  infrctir 
tiivved  by  a  rapid  li-rminnlion. 
spinal  fluid  obtoined  hy  punet 
slowly    (days)    extends. 


I 


iraeler 

"tie  svmplefti" 

re  uielnr 

svinploms  beni 

line   Iiilal 

Pin.il 

pilrpsy   {48a). 

In  early 

*  of  muscle  sense  a 


Tlirre  ii.  paralysis 
always  of  motion 
and  commonly  of 
•ensalVm.  usually 
in  the  form  of  para- 
plcBiii,  mon-  nirfly 
iu  the  (opin  of  a 
spinal  hemiplegia 
(432),  which  later 
may  breomea  para- 
plecla.  The  re- 
Hexed  are  exasfier- 
ated.  Anitle-elonuf 
and     RabiiLskI     are 


Choreic  nymploms. 

Oninial  and  spinal 
nervos  arc  la- 
volvwl. 

Lrms  and  legs  arc 
paralysed.  Pri- 
apism Is  com- 
mon, also  re«- 
piralory  difficul- 
ty and  eariy 
death.  Radiating 
pains    arc    com- 

I 


I  or  aooompaniee  on  attack  of  hemi-chorea. 


a-medullary  I 
ivolving  the  » 


'   positinn  of  liic  tumor. 
I  produ"e  irrtlnlive.  ini 


of  ibe  bod.v  :  witli  nnalcesia.  thermic  and  sometimes  tactile  anesthesia  nf  other  side  (432).     Stationary,  or  sfendilv  pn 
Thev  may  lie  absent,  hut  are  usually  increased  on  the  side  of  the  motor  paralysis,  nnrt  are  so  greatly  increased  freque 

pr-m'-dullnry,  |iiiral,vtic  symptoms. 


•  ressive  ebronic 
illy  as  <o  cause 


e  side  of  the  bfsly.     Symptoms  mny  be  bilaternL  nut  are  Ihen  dilGcull  of  recognition.     In  many  cnfccs  the  hj-polojiia    (almost  i 


The  parnlysiH  !■  only  sllirht  and  folku 
a  paralysis  (choreia  mollis). 

luieitfion  frrmilr.  nj-»tasmu».  scanning  speech,  ataxia,  irregularly  dislrlbuled  molor;  and.  rarely,  sensory  paraipiis.     CTironlc  course.     Tiien-  ma.  be  opiic  neuritis,  vertiio  and  app-iplwliform  ntlnck* 

There  may  be  a  history  o'  injury  and  a  fracture  of  vertebnc  with  der«rmily.    The  knee-jerk*  may  he  abolishwl  in  the  early  stagea.  Inlep  incivascd.    There  may  b.  Mowl  in  the  cerebro-spinal  fluiiJ 

No  hivtory  of  injury,     l.iiile  or  no  pain.     Sensory  symptoms  and  dlsordent  of  the  organic  reflexes  are  almost  always  preaeni.     A  history  or  other  evidence  nf  syphili*  (1205)   is  often  present  in  <-; 
litic  myelomalacia  (1211). 


I  May  be  history  of  remote  iniiir.v.    Much  pnin  radiating  into  arm 
lluid.    In  early  slages.  exiw-medullary  liimorx  produce  liritnti 


.  Mu'-I 


and    riffidilv 


and  -L 


sent. 


Spnsr 


and 

often  present.  The 
motor  paralysis  in 
pcrmaneal  or  lasts 
a  very  lone  time. 
Sensory  paralysiK 
msy  be  slight  and 
transitory  and  may 
be  altogether  ab- 
sent. The  aneilbe- 
ria  U  often  limited 
abin-e  hy  a  narrow 
<onc  of  hypi>rc«lhe- 
■ia. 


[■ains  radlatin; 
into  llie  eitrfW- 
ilien  are  mmmoB. 


Legs  mainly  in- 
volved. Arms 
in\-nlvi>d  later 
and  sitehtly.  If  at 
nil.  These  dis- 
eases may  occur 


e  may  be  a  history  of  injury  n 
islory  nf  ininrv.     Little  or  nn 


b-  a  hi. 


..ry  of  r. 


ex  Ira -medullary  tumors  prodi 

Eiideiire  nf  Pott's  disNI«e  or  tumor 
nain,  In  coses  of  compreurinn  du* 
iiti-r<'a«ed  |rn>inn  and  may  roniain 

History  of  workin::  under  ineri'oiied 


Inlra-meiliillary  paralyll 
nd  a  fracture  of  vertebwe  with  deformity.    The  knee-jerk^  mi 
pain.     S-nsory  symplonis  and  disorder'  of  the  organir  reflex 

Much  girdle  pain,    Riddlly  nnd  aoasm  in  back.     Symptoms 
irritntjvc.  intra -medullaiir  paralytic.  s.\-mptoms.     ^Tiiscle  spasn 


ii*m  of  bnck.     Symptm 
iploms.     Muscle  spasm 


!  nt  fir^if  more  ui 
is  characterislic. 


V  be  abolished  in  the  early  stages.  later  in-r 
s  are  almost  alwn.va  nrrBcnt.     A  history  or 


liint-ral.      I.ni-nl    rmini.      Mny    b-    increasci    lenision    of  ei 
Rnhinski  present. 

I'li-re  toav  he  blood  in  Ihe  c«rebro-npinal  fluid. 

vidence   of   syphilis    {12(K)    Is   often    present    i 


Patients 

re  nmotional. 

Very  acute  onset 

es  of  syphi- 

/Acute  onset 
1  rhmnic  onset 

rehm-spinal 

Very  chronic  onset 

\*ery  acute  onset 

n  syphilillc 

r  Acute  onset 
1  tTirnnic  on»et 

■■erii.vil  recion  of  spinal 
eord  above  cen-lcat  en- 
larcement.    (PNg«.24-R.) 


;  first  unilateral.     f/>enl  pain.    The  tenai'm   of   Ihi-  cerebro-H|ilnal    fluid   i 
is  a  characteristic  symptom.     Rnbinslrf  is  present. 


>  he 


.P.1,      Tn 


stage*.        Very  cliri 


ins  Ihe  cord,    Riddily  and  sintson  in  muscle 
s  disense  there  moy  be  no  aenKory  nymptoma 
I  and  exhibit  lymphocytosis. 


of  l"os  und  haeli  nr 
Reflexes  may  be  so 


'  friinirnl.     I'sually  intense  pifn  wlien  spine  is  bent  nr  r 
■snsgerated  as  to  conntitute  spinal  epi]eps;y   (fW-l,  43.1). 


nd  cflperi.dly  or 
V  according  to  s 


DIAnNOSIS 

Vr.-bral  Palsy  of  ('hi)dli<HMl,    Porenct'phsly,     ,\cutc     501 
''nisiphaliiiv      Infantile    hemiplegia    or    diplegia 
(I,ittle'»  .lSea*el.    (117.  .177,  1114-31.  SOI.  1051. 
lOKS)      (Fig*.  l.Vin.) 

>Ii>nint;eal     .Vpcplexy.       Hemorrhage     in  ^'rebml     502 

mnnlnBe*.        I'achymeninsitis      Interna  llemor- 

rhari'-ii.      Amiirism.   etc.      (.'>SS.   tO«S.)  (Pigs. 
1,-1-111,1 

'iT.-bnil  HcmorrhiiBe. 


504 

Cerebral 

acute  f  Apiqilexy.  > 

I    (147.  l."!*.  422,  .VM. 

SJf.,      SI50-1.      1043. 

lOiH-fi.l 

(Fic».  ir.l7  1 


Cerebral   Throinbm 
«oftening. 


•N'o  fever.  No  infection,  or  origin  for  abscess.  Chronic  coui-se.  Steady  progpesslon  of  all  symptoms.  Often  histnry  of  previous  remote  injury.  No  in- 
of  pellular  eb-menls  found  in  the  blood  or  in  cerebro-spinal  fluid  obtained  by  lumbar  puncture,  Frenuently  symptoms  are  irritative,  rather  than 
lir.  I'ercuKsien  of  skull  over  region  of  tumor  often  shows  (endernes«.  H>'adaehe  is  very  rarely  absent  and  is  usually  intense.  It  may  he 
I  or  local,  hut  is  of  'ittle  or  no  value  in  localijiins  the  tumor.    The  panilj-sis  crmmenecs  as  a  monoplegia  nnd  very  slowly  (weeks  or  months)  ex- 


I.  especially  suppurative  discnsea  of  the  ear.  Rapid  rcurre.  esrepl  that  a  Intent  neriod  in  the  progress  is  common,  fol- 
nelirium  is  common.  Often  a  flistory  of  a  recent  injury.  Teumcvlcsis  mny  be  found  in  the  blood  and  in  fh"  cerebro- 
re  (741.  Frequently  sj-mptoms  rather  paralytic  than  irritative.     The  paralysis  commences  as  a  monopleein  and  rather 


'cnbnil  'nimnr.  Uleuiititie  Cyst. 
(bV.-.  nil,  .■S.VMMl,  r.7S,  .1S7.  R3«.  S,'i2-0-4(2-4-r. 
'MS-'X  Otll,  inai-riO.)     (Figs.  16-17.) 


■er.tirit   .M.-erw  .ir  |nr:illjie.l  Meoinnill.,  MS 

(I.V{.    171.    l--!.   ."uS,    ,-,S7.   907.   tXll.   1X17,    Ifllf).) 
(I-Vs.   1-V17.) 

Spinal  Tumor  or  unilateral  spinal  b-*ion.     Brown-     509 
Senunt^l  -  paralysis.    (IM.  101.  4.12.  +*«.  r.lB,  GIO. 
r.4l.  .V.2.  R2.'^:t!l-44.  !)i.*i.  0S2.  100ft.  127il.  1405.) 
(FIk*.  24-1!.) 

<  hon-ic  Paralysis    ((^.)  &10 


l>i 


seminatetl  Sch-nwls,     (l.'iO,  TiMI.  tV<0.  OCR.  ASS,    511 
.■|0.  70.S  M>3.  014.  inM.) 


Injury 
.\c-ule 


l-um 


Injury  or  lieiiwrrliagc  in, 

,\iiite  myelili^  or  myelomalarin  of.   (7itS.  Sill) 

r'lironic  myelidi  or  myelnmalaria  c^f. 


merning.     Much  cinli"  pain  and  rodlatini: 
e  msy  oociir.     Orebro-apioot  fluid  is  under 


Old  Bse.  aiheromatous  arteries. 


iiapheric  pressure.    Headache.  Terliro  nnd  vomiting  in  early  ntngc  of  diaease.     I^ler  symptoms  n 
irlerial  lenslon  usually  high,  loss  of  memory.     l'>iintional  and  exbiluis  mental  impairment.     Paral.vsis  is 


Tumfr  can  be  seen  or  felt  on  back  replacing  the  spines  af  the  vertebrae, 
fvr  not.     Clul^-foot  is  common. 


r  the  cleft  can  tie  fell  in  spine 


lins    and  paralysis  of   legs.     Some  cases  exhibit  an  apoplectiform  course  with  cmia  and  death 
evere.  resembles  that  ot  pnrnlyis  agitnns  without  tremor,  and  rciiexes  of  all  kinds  are  not  much  altered 
There  may  not  he  paralysis.     Ileflexcs  mny  be  present  or  exaggerritctl  according  a*  the  lumbar  enlarHemet 


<*<ii-.4on  diseace  or  Diver'*  paralysia. 
S-nile  Parapl.gia.     (7IM.) 
S|.ina-bl(ida.     Il02.) 


4S1  » 

Paralysis  of  any  ex-  Pnnily-li       limtl..l    ■ 

tent:    IoimI,    ninnO'  by  some  pinmiui'CLi 

I  ple^Ia.    Iieaiipleiia.  aoalomiml       laod- 

or  paraplegia  mark. 


mia. 


ffvere      nne- 

( 


degree  and  disappi 
T,cgs  off. 


:reat  resistance 
thi>  «rly  stBge 
'pt  perhaps  hy 


lie  muliir  parnlfl-  i 
i>h)-4irian  (imagina 
diirntion.  Orgsiiie 
nieots  (4:ttll  |  do  n 
In  walking  Biitewa) 


■ilallon  predominate  over  inose  of  paral>-9i8      Much  rigidity,  girdle  and  radiating  pains  and  spasm  In  back  mnsclea.    There  la  usually  spasmodic  retention  of  the  urine  in  earlv  stasec-     Paralssis  Is  of  sudden  onset  slight  ii 
■  -ord  IS  involved.     Usually  a  history  of  injiirr.    Reflexes  ex  .ggemlwl.     I.uml.ar  puncture  may  yield  a  Woody  fluid.     Svmptoms  vary  with  nnsition  of  h-m-rriiage. 

Pnrnhsis  purelj  tnotor,  a  paresis  rnlher  than  a  complete  paralvVw,  very  slowly  orocr-^ive  and  oft^n  sintinnnrv  rliirine  lone  neriotls.     Snasm.  rigidilv  of  leg  mnsi-l.-.  and  later  contraclures.     Kn-adr  exatraerated  reflex-s. 

10  (.a«ive  luollrn.  '7r''«n"y  wlien   rapid      Ankle  clonus.  Rabio«ki  nnd  ^ninal  enllonsv   (4331.    Or-anic  reflexes  little  if  al  all  disnnlered.    Arms  usually  nnt  nffected.  but  may  be  sligbtlv  so  aft^r  years.    This  clinical  pirtui 

11  M  nt         '■re!-    jT  w      .      wIj  1      "'^'""'  ■""■"''"''■'-  nlthoiieli  in  it  H>e  r-flexe*  arc  not  always  irr-atlv  exmrgernle-l  and  the  posterior  columns  ore  at  time*  involved    cannot  he  distinetiv  separated  from  thi" 
<s  ciioi  .y.    i«iM  nis'.n.e  may  he  simulated.  !n  a  very  mild  form,  vvilh  exaugcrated  knee  jerks,  but  without  ankle  clonun  or  Rnldnski.  and  with  marked  stiiTness  of  legs,  ns  the  result  of  reflex  aetjon  from  Irritation 

There  is  n  comtunntion  of  motor  paralysis  nnd  markcl  ataxia  which  develotis  very  erai 
and  Rabinski  ar-  preseni.     In  snme  cases,  espeHally  tow  ml  the  end  nf  the  diseas"  tl 

ra'l'mir'i7!^.'"i  "   l"^"^"'  Y""'''!^'  "'"''"""'■>■  *>■""'''""«•     T'"'  disease  1-  usually  of  sudden  cnsi-i  ami  ofieu  follew<  seme  powerful  cnioliim.     It  is  usually  permanent   until  cured  by  another  Bimnc  emotion,  which   mav  be  oftrn   artifiHnlk  pr-slueed   by  the 
.    .1  paraiyse.1  limb  otten  olTera  great  re«istan<-e  to  pnsnive  motion,  even  to  slow  mollei.,     <-..|itrtieiiires  ai-"  iwnmon.     Knee-jerks  are  usually  incr-n-ed.  but  no  true  nukle-clenus  cr  Unbin-'ki.  the  ankli-.bno^  lielng  either  ab*cnt  nr  of  <hnrt 
.common^  HjKierienl  symptoms  (4l.'il.     ImpoBsibilitv  of  exiil-inin*  all  cf  the  «vmptoms  hy  snr  one  orennic  lesion.    The  paralysis  is  not  limited  to  one  muscle,  or  to  the  distributinn  of  one  nene.     Ass.ieinted  move- 


llrr 


in      *pi> 
riincbis,     (n(W,  073.) 


lal      mcmbrani-s.       Ilemato-     Sil 


I  rarely  there  r 
iski  prp-ists.     1 


j**lhe»ia  and  analgesia.    The  tendon  reflexes  a 
s'ase  of  ndnit  life,  but  is  analosnus  to  Friedre 

Bifonc  emotion.  i 


especially  from  Ihe  ge 

•arly  stage*.     ,\nkle 


Spastic    I'amplegin    or    lateral    sclerosis     (usually    5"J5 
symploai  iiic  nnd  part  of  a  mon-  extensive  lesion, 
•n.innl  or  cerebral).     (547,800.)     (Figs.  24-7.) 

Ataxic  Paraplegia  or  poslero-Iati>ral  .flerosis.  526 

(ili».  lOn.)      (I'lgs.  24-0.) 

IIy.terinil  Paralysis.  527 

(747-.'*.  7li2-!H!.  WO,  lOTU.) 


stepping  laterally  along  a 


r.enl  pan|i)--<ii.  and  this  Is 


itraighi  Hn 


limee  of  mine 
tiysterical  hemiplegia  the  pat 


'Is.     In 


walking,  in  organic  hemiplegln.  the  leg  is  swung  outward  nnd  forward  in  an  arc  (mowing  gait)  :  white.  In  hjrsterical  hemiplegin.  the  paralysed  leg  i 
Iks  badly  in  each  direction;   while  in  organic  hemiplegia  the  patient  wvlks  well  towards     the  paralyaed  aide,  bul  badly  townrds  the  healthy  side. 


dragged  • 


■  after  the  oih'r. 


v^ 


CHART  Xb 
Spastic  Paralysis 


Comprising  Numbers  478  to  481  on  left  side  of  Chart 
and  501  to  527  on  right  margin 


137 


o* 


DIAGNOSTIC   ANALYSIS   OF  STMFTOHS 


DIAGNOSTir    SYMPTOMS    AND    TESTS 

f  Bilntfnil         Bymp-      If  Ihe  paiknl  dons  not  promptly  dj^  one 


ABSTRACT   OF  SYMPTOMS 
cninifil  dW"  -^  pn niljsed.     There  i*  mori-  or  l<'w  mnrkril  spaRlic  pnraplc- 
eid    (32ro.    There  are  iiitiiallj-  dj-Biirthria,  dysphaeia.  ,l«xli.  ■'""tli'-sm  nod  ofien  vertieo.     (Iliilbnr  symiiloiiis— JM.)   Symp- 
toms »t  firsi  roay  be  mure  uniUtwal. 


CniitBl     nerTci 
itlnne  invnlrwl. 
(F>e>.  IS,  23.  33. 
38.) 


TrniBiyl  pnrfllTsiB 
(2-'><I)  nnr)  hnlhar 
v<iyuiptom»  HS-l). 


r  more  vye  mtiMM  of  onr  n'uU-  nod  o(  nno  and  li 


i:  of  nppii>iil<;  side. 


Paralj-si*  of  h^-poslossiu'  of  <mi-  siiii-  nnii  i>f  arm  ami  li-e  of  opp  "i 

A  disease  i-nii:>ed  hy  r-ntin^'  iipi>ilril  fiiod  (sniisaife.  pnrk,  cbf'*''' '"' 
even  aplmcia.  Tlic  nio*l  eharaeleritdJc  siymplom  it  oi-idar  pnr,i1j 
e^pci-Ullv  Hif  exl'muf,  are  parnlyxiil.  At  the  flulnpty  the  Ittol'  r 
paiinn  i<  n  pi'irniuettl  nyinplim.     The  disease  hoK  n  very  h'^l' 

The  onset  of  pnrnlyHi-t  in  sndilen.  If  the  patient  d«>"s  not  die  promptly.  Inter  tlie  sjinptoms  are  rwrrewiive  rnthtr  than  pro- 
grewive.  lliey  iin'  uKunlly  nniliih'ml.  but  mny  }«■  bilateral.  A  number  of  motor  cianinl  nei^rcs  nre  paralysed,  while  there  is 
a  spnstie  pnrnly«i»-  more  or  lew  proiioiin<'"'«t  in  the  anna  andl'^e^.  Verlico  iji  a  eemmon  symptom,  May  be  due  to  n*nite  in- 
Unmmntion.  Iiemorrhnse.  thiYimbosin.  eml>nliEm,  or  rv>mprearion,  Alny  oeeur  in  ncule  (interior  poliomyelitis.  Often  due  to 
syphilitic  endnrlerttis  or  syphilitic  nouritis.  or  to  aleohol  or  other  piiisens. 


eil   food,   pTo.I    ond   therefore   owurs   in   sroiip*  of   persons  who  bni 

Anihiynpiii.  diplopia.  pI'isiB  and  rnydriaHiB  are  alnnyK  pri'sent  and  often 
raniiil  noelei  are  found  dinensed,  but  the  spinnl  nerve  ei'llsiiri'  not  involve<l 
)rlnlily.    iind    ik    due    to    Ihe    ing<'Rtion    of    the     Bacilliig   Bolulinu^. 


[■Acute  onset.     Resr^si"e.     No  optic  neuritis.     A  variety  ofapoplexy  (504),     No  increased  lensirm  of  ecrt-bro-spi 
\Ohronii'  onset.     Progressive  course.    Optic  neurilia.     May  beiuerea»ed  tension  of  cerebro- spinal  Ouid. 
f  Acute  onset  and  regn-ssive  couise.     .^"o  optic  neuritis.     No  increased  tension  of  ccrebro -spinal  fluid. 
^Chronic  onsol  and  progresaive  course  and  optic  neuritis.     May  be  increased  tenakin  of  cercbro-spioal  fluid. 
rAeoie  onset  and  rcgreseave  course.     No  optic  neuritlR.     Noincrea»cd  Icnsiuii  of  cerebro-spinal  fluid, 
[rhroiiic  onset  and  progressive  course  and  optic  neuritia.     Mny  be  increased  tension  of  cerebro-spinal  fluid, 
onset  nnti  regrewivo  course.    No  optic  neurille.    No  'nereased  tension  of  cerohro-^pinnl  fluid, 
onset  and  progressive  course  and  optic  neuritis.     Mny  be  intireased  tension  of  cerebro-spinal  fluid, 
louethi 


r.Vciitc  0 
1  Chronic 


The  fipKt  Hj-mptoms  are  prostmtion.  nr 
in  an  exireine  degree,  'Hie  pupil  is  immobili 
■ither  cltnicftlly  or  pathologicwily.     T 


ttle. 


a  and  vomilini;  followed  by  dyanrthria  and  dji^phatHa  or 
'onmmo'lalion  is  lout  and  one  or  more  of  the  recti  muscles. 
or  no.  mental  disturbances  or  fever,  hut  obalinnte  const!- 


Th. 


ia  more  or  lf«  extensive  purniysia  of  Ihe  motor  nerves  --f  i>yebiill    f.Srd.  4th  j 
vision.  nyntoBTnus,  etc..  may  result. 


1  Uint   ptosix.  siguint.  double 


There  is  paralysJ!:  of  the  lips,  toniruc.  pharyni  and  larynx  tTih,  Olh.  lOtb.  11th  and  12t(h  nerves)   with  conaetiuent  dysa 
HiPin  and  dyspbnpin  and   umially  ataxia  and   respiratory  diaturhaneefl. 


itiliil 


Thi-     c'hprinie     fomw    of    tliese 
:,  with  ttie  spinal  form   (fi47-P) 


the 


•11 1.-11 


airophiw  and  resemWe  the  musnilnr 
d)titropbir»i  in  that  the  pnrnly.si':  anrl 
atrophy  advance  tocether  slowly,  and 
it  in  diflinilt  to  «ny  which  is  primary, 
■niry  nlno  mnstitiite  n  group  of  (Tronic 
deeonwative  atrophies.  The  paralysis 
is  purely  motor. 


[The 


paralysis    in- 
«  the  eye  raus- 


A  irrsjdui 
plesiii 


I  onset  of  wcnknews  of  onilar  muscles,  H  may  be  steadily  progreMive 
■yriwll".  immoliile  p"pils.  The  disease  may  nttne';  nnly  the  e»t"mal  nm 
■miiletii  I .     Dispnsr  may  be  complicated  by  biillmr  paralysis  f."i4'!l  and 


ir,  hnvioc  procressorl  to  n  certain  point,  it  may  remain  stntionni 
,ele«  of  the  eyeball  f"pht!ialmoplo?ia  external,  or  only  the  ioliTO 
s  iiaunlly  niaweiated  with  mnj'olrophic  lateral  acleroaiR. 


Mu^i'lra  mny  lie  attacknl  in  any  order,  ptosis,  aiulnt,  im- 
mui<-les    (ophthnlmoplesin    inlernn).    or  both,    (optitbalmo- 


riir  pumlysis  in- 
vf^lven  the  lips. 
Ifincue.  pharynx 
and  larynx. 


iiili«  Ii«dI  fiirward.  Tbnre  are  hulhor  symptoms  (4"I),  Thcr 
1.  pharynx,  Inrynit,  etc.  Roth  facial  nerves  are  invidved  in  s 
■<-ii'-e  of  advnncod  life.  Often  associated  with  amytrophie  later 
II  due  1.1  leeion«  in  both  eerchrnl  hemispheres  in 


r  len  mnrk-d.    Tlicre  is  more  menUil  i 


are  ilrcolinir  of  saliva,  dysarlhrin,  dj-^phnyin.  and  nphoi>ia.     Paralysis,  tremor,    atrophy,    (ihrillnry    cnnlrnctinn    of    niriselrfi    of    toncu''.  lip*. 

nic  e.iHcs.    The  pnralj-si^  very  simvly  pmcressew.    There  are  syTOpiomnnt  a  mild  spasric  paraplcRin  in  lcp«  with  ankle-clonus  and  Rnbinski, 

1  sclerosis  and  nt  times  with  proiiressive  ophTbalnioplcKia    (fWal,    In  addition  to  ibe  pseiido-biilbnr  pamlv^is  of  mynithonla   Bravis    (n.'Ml 

k'hich   thcri'  li  no  miincle  atri>ph,v,  or  librillation.  and  no  change  in  the  pleetrienl  reaction,  but  nil  Ihe  other  symptoms  of  bulbar  paralysis 


i|wiin 


nt  and  k renter  emotional  exeilnbility  tlian  In  true  bulbar  paral.vsla. 


'Pymmetrlcal  pnra]- 

I  the  Kmnll  mnm-le 
!  of     iHuidn     or     in 

I  Mionlder      c  i  rd  1  e 

|Synmiotrirnl  para- 
:ly«i;i      commeneinc; 

I  in  Ihe  muscle*  of 
the  IMfAs  and  but- 
tock*. 


^(•le«  ,i(Ter'|ed    f^hin 


iie  weflkncRS.  atrophy,  fibrillary  contrnciion«  and  nil  doerees  of  alteration  in  electricjil  «cHtaihil|ty  from  simple  diminution  to  complete  reaction  of  di^nn.- ration.  The  pneres 
m-]e<i  of  the  iJioubler  girdle  f ecaniiln-hiwneml  Intel,  is  usually  fairly  aymmetrieal  a-d  extends  to  the  other  sroup*  of  mu^les  in  arms,  hody  and  even  lees.  The  muscular  w-iikr 
■oiiirhl  across  hand  to  touch  ihi-  lii  Me  linaer.  The  fineerH  c.nnnot  he  spread  apart,  nor  can  llieir  last  two  phiilanire<i  he  extended  on  the  first.  Th"  less  show  n  m'ld  dej;rre  of  spa«li 
arc  Kw-ondnry  ennlnictureB,  i--i»'ciiiil.\  111.-  "clnw  hand,"    The  hivid  is  usually  bent  forwaivl  ind  there  is  miiHi  di'formity  nlKiiit  the  shoulder  and  olher  parts.     A  disesise  of  adult  lift 


at  initnliilily  of  iiiuseleB  is  incrensptl.     Often  nssoi'laled  with  |iroi;rfKviii-  hulb-jr  pnnilynis   (.54*'0.     Some 
end  I'liliiuuif  are  involvr-d  'or  not.     It  i&  dillicull  to  draw  any  ■iui-li  di^liaelion  clinitiilly.    Tlic  one  form 


nlhors 


ay  ti 


into  two  irroups  according  as  to  whethir  theiitr-ipliv  or  the  pnnily*!! 
The  symptom  complex  is  divided  into  two  gnnps  (.548)   in  thi«  chart. 


Samp  sj-mptoms  as  above,  but 

This  rail-  diseane  commences, 
end  of  a  few  .vears.  The  n 
tory  lesions  and  without  nr 


•,  symptoms  of  lateral  sclerosis.   This  disease  has  lieen  ri^ardH  as  n  chronic  poliomyelitis.  Tlie  two  disenscs,  however,  differ  rnilicnlly 


primary,  and  as  to  wh<>ther  the  Int- 
ioto^ically,  patholoKlenlly  nnd  elinicnlly. 


in  the  brut  or  second  yaf  of  life,  with  a  oymmetricnl  , 
usrb's  exhibit  the  rcnelloa  of  deff»neratioii  nnd  little. 
y  in\o|vment  of  Ihe  pyraniiiial  tract. 


trophy  of  Ibe  muscle"  of  the  thiehs.  polvii  and  bin'li 
r  no,  pseudo-hypertrophy.     The  lesion  consists  in  an 


.'rndually  extending  upwards  and  downwards,  finally  intolvini:  the  hulba 
trophy  of  the  nerve  cells  in  Ihe  anterior  horns  anl  a  dee^nration  in  the 


Ma  rkeil  scninry 
•ymptoini  an*  pres- 
ent, sueh  as  pain, 
parMtlifwae,  anes- 
th<WH.  i-tc.  with 
the    mutor    pnraly- 


nolli  amx  .ind  lre»  are  pamlyHod.  There 
are  irojihic  disturhancMt  in  Ihe  armn 
and  not  in  Ihe  Ices.  Pupils  are  often 
nnniuHl.  It^-HeiCR  are  abolished  in  the 
arm*  nml  increased  in  the  Ifcs,  nnb- 
innki  and  anblecloniia  are  preaenl.  The 
bladder  i*  usually  more  or  le»B  dis- 
ti-ndfil :  iin  detnisor  beinc  parn!y«e«I. 
l^'inirMiliin-t  may  be  present  in  the  leEB, 


eule  onset.     Syinpton 
yield  a  bloody  fluid. 


c  mo*t  extensive  in  first  few  days  and  t 
:.    Symptoms  conlinuc  to  extend  for  sim 


xlowly  improve  later.     Stay  he  dejrrrmity  in  cen-ical  region  of  spine.     Knee-jerks  mny  be  absent  in  early  stages.     I/inihnr  puncture 
me  nnd  are  fnirlv  symmetrical.    Orcsnic  reflexen  disordered,     A  history  or  otlu-r  evidence  of  sj-phUU  (IGCIl  Is  often  found  in  syphi- 


I  and  fi|insnH  in  nrm^ 
lae<*s,  spastic  symptn 


nnd  neck   prei'ede  thf  pi 

IS  appear  in  the  lept. 

if  chronic  syphilitic  m^-r 


nnd  a  pmareMilve  course.     Symptoms  at  firat  mainly  unllatet 
!  piiralytic,  lymploms. 


■  and  c>riiiiiici,ure!<  and  mii^i^ilar 
wus  eni|>tionK  (herpes,  pemphie 


itrophy  in  hands,  "daw  hand."    The  flexor  muscles  arc  more  completely  parolysed  than  the  es- 
•.  elc.)  are  not  uncommon.     Pert  bro- spina  I  fluid  may  he  under  increased  tension  and  show  lym- 


Pi«rebro*pinal   flufd  mny  shoi 


ical       enlarite- 

1      of      spinal 

(Pigs;.  M-e.) 


(»; 


n  nf  m 


AM   th-   miiM-lM   of    Tlir 
the  body  and  hefld.        mi 


inwii'iatien  of  sensniion  is  the  most  i-hanicteridic  nj-iuptiim  and  is  cnnliinnl  with  uiiin  -ind  pa  rent  hen  in  e  and  more  or  low  mnlor  paralysis  ami  atrophy. 
Trophic  le«ions  are  usually  piv>minenl,  Pemphinis.  uh-emlion  and  ni'ilil.nii''"  of  the  hanils  and  Imphic  lesions  of  bones,  musclett.  and  olher  lissuex  oecii 
trophip  svmiitoms  predominate  over  motor  symptoms  in  Ihe  arm^:  while  thel-i-B  nhow  a  mild  fpastic  pnrni<le(ria  (.">2,"i).  and  sraliosis  nr  k)'riho<ii>i  "nui 
prr*»n!  the  sj-mplnms  may  he  twth  in  arms  and  lees,  and  the  motor  ^vrnptcpnis  an-  iibnul  ak  pnnnineat  a«  the  sensory  nnd  may  he  nnilitr-ml  in  thi-  ear! 
cerateil  In  ■■"nlral  allfwiis  in  Ihe  cervical  or  donwl  region*.  The  cen ical  form  of  the  di^nii;-  runs  a  chronic  course,  exlendinc  at  times  ovit  dead"*,  but 
r.ipid  ennrw,  and  may  exhibit  a  unilateral,  spastic,  muscular  paralysis  nt  lea*!  in  the  early  slaae*.     In  sudi  eases  the  lesion  cnmmen  eii  in  the  Iinulint 

■"Ijl,''''''"!,  j"""  r'  **''  '•''"■"■«'  '»  "'"  "pi'l  tirine  of  the  mui.-b'«  whm  in  action.     Piiiinil  can  walk  w-II  at  the  slnrt.  hut  after  a  few  forn  fow  bundredl  sfrn.  i*  Iind  eut.    The  «amp  is  tnie  of  all  -ithi-r  volunliiry  acts.     Kvuniinnlion  of  the  nius.dr*  with  el-clricily  Kive«  the  ms-B-lhenii-  re- 
t.fln»l.     There  I.  no  DiuHnihir  atrophy  and  no  rvnction  of  de'i-ncration.    In  the  domain  of  eninhil  nerves  fin  whirti  the  en.sc  usually  coinmeneisl   there  may  be  ptoslw.  diplopiPi.  ophlhalmopleBia.  diplrgia  facialis,  dysarthria,  dysmasfsia.  etc..  and  nil  the  spinal  nerv<»  may  hp  affcctod.  The  Iwad 
of  the  ptOHia.     "nie  nymptomsarc  slight  in  the  niornin?  and  «mw  worse  during  Ihe  day.     No  sensory  dislurli.inees  cscepl  painful  cinmp".    Organic  rcflext-s  normal.     A  tumor  is  often  found  in  the  thymus  gland  and  multiple  foci  of  small  round  cells  (lympbo- 


e  muKciilnr  atrophy  haK  often  the  location  nnd  char;< 
1  Ihe  t.viiP  called  MonanV  disease.  In  the  most  comn 
I  mere  tb"n  half  the  cases.  Pnnidnxicnl  fS7I»  and  -. 
aees.  All  forms  of  ri-flex  action  are  abo|ii;hefl  wh^n  I 
iwly  prosretses  and  the  anefllhesia  at  first  sliBhl  si'ai 
Uiruemcnl  and  aetccnds.  prodiicinc  tlie  nymptnms  simt" 


■riiticB  of  that  of  proEre>i>.ive  spinal  mnseular  atrophy  (MS). 
I  form  Ihe  c-nieal  reeion  Is  alone  affecteil  and  si-nsiiry  and 
nianooiis  sensations  have  been  noted.  When  a  diBHise  clioma  is 
rprvieni  and  lumbar  enlarsemcnts  arc  Involvetl,  hut  are  exag- 
i  hecomps  more  nmrh.<1.  Tlie  diffuse  form  often  runs  n  fniriy 
at  resemhlinit  a  very  chronic  aia'endini:  paralysis. 


I*  held  reimclivl  t\ 
t  lb.'  Miuspirs  nl  the  autopsy. 


Mn«-lp.   „t   one   or 
holh  lees,  rarely  of 

lofmiiti 
Rarely 

rommnnHnc  in  lei-i 
exlendinc    to   arms. 

but  in 

Aikocialed    with    a 
<-rvinil    rib. 

li«.  sk 
ralsia. 

.\«n.in(«l             will, 

arterial  disMte. 

ReppBtrn 
of  per 

■Ml  "V"''"  "'  !'■''"';'■  ' iIp  cmmp.  nnd  iveakneat  of  leg  or  b-s«.  cnuwd  by  nalkina.     Putini:  the  allnck  Ihe  feet  are  cold,  and  there  is  diminishcil  or  absent  pulcatii-n  in  arteries  of  fe*t.  aiw>ciat"i  with  marki^  arterio-srlen'=is  of  arieriefi  of  leg  .is  shown  by  palpation  ami  by  Ihi 

e  r  in-Atf  occurs  m  one  or  both  arms.     No  sensory  distur'ianc*'  except  painful  cneinps.    Orgnnic  refli-xi".  nonnnl.     Ancio-spnstic  hemiplcKin  in  which  Icmponiry  attacks  of  hemipleeia,  sometime^  associaled  with  aphasia,  occur,  is  probably  a  variety  of  this  disease. 

"nil.""'!"'  »  m!"^!*'*^!"'  '■*""  '""'"'''■"  "^  '^''  ''■^  usually  firnt  nnd  then  of  arms,  laslinn  a  th.  hours  or  day-,    llie  attacks  usually  ocnirin  IJi-  morning  er  after  rest.     During  the  attack  the  left  cardiac  ventricle  mav  become  icaipornry  dilatwl  and  n  murmur  mny  be  beard,     Tlie 
an  IU.1  .lunckpu      i-hern  i*  usually  well  marked  heredity,  or  Ihe  dis.'a»e  occurs  In  family  «r.'iips.     Durine  n  »cv.-re  altnck  three  is  often  a  diminution  or  nb«i>n<'e  of  the  i-eflexe*  nnd  of  the  fanidic  and  galvanic  excitability  of  the  aerve?.  ami  of  the  mechnnical  cxdtabiHtv  of  the 
tr<.iips  01  lamily  perioiju-  paniljwis  these  negnlive  symptomh  mr  not  preseul.     Soiu?ef  thejc  cfls,»  on    apparently  dur  to  malari.i  and  can  Im-  curiil  by  Ihe  adutinixlnition  of  quinine. 

in  «!,'  7"J''  **"''  ""r'  '"""u'"'  '^''"  "^"'   """   '''*"*■■      '"  """*"•«'"■-  ff  n-rrii-ol   rib,  nttncto.  o'tnir,  hm   only  afler  use  ,.f  the  ana.     Tli.-w  attacks  are   i]i.ually   unihtteial.  ev.n   though    Ihe   extra    nh   U  on   both   sides.     TIip  attack  ronsists  „l 
,n,.  il  V-    ' Vli  "  ,  ".""  .""*  ^"^  ""^  "  "*""■*  •■'"''•  "'"'■  '^  ""■  "f  '^''  """  '"  ■■'">'»""•■''■  ""•  «""  "'""vs  a  dcHdeH  panels,  which  pas,.--  off  if  Ihe  arm  U  kei.t  at  r-.t.     An  ununited  fracliire  of  the  clavicl-  will  rnr.-lv  .Miisr  simil; 

.  maj  w  caused  by  a  cervical  nh.  and  is  often  n'liev.d  by  elpvalion  of  the  arm  and  it-  n>"'le  wocp  by  motion.     In  rare  cases  this  parnlj^is.  ai  first  i 

rl  allarln  „(  trmporary  pnml.vsis  are  very  rnrelv  met   wilh  inbv.teria  and  In  eld-rly  per«ont  with  thick-n<-d  arte 
.•Oral  oriKin  euch  paralynwj  are  of  limited  extent ;  when  of  spins],  gen-ral.     See  al"o  oeeupition  neurows  (615) 


.  in  which  cases  apopic 


ly  unihiteial. 
arm  U  keiit  al 
lermiltont,  ma 

V  is  probable  Inter.      Some  ci 


e 


DIAGNOSIS 

ni'morriiage    softening  or  anite  infiammation  in  brain-stem     R34 

l,-.i;t-4.  Wtl.  7-I01. 

Tumor  ill  or  eomprpwinj;  the  bmin-slem  (aFjtl),  fi3o 

Ilcmorriingc  or  xoflening  in  crii-i  cerebri  (r^lS]  fiSG 

Tumor  in  or  comprcHsing  cms  pprehri   (fl5G).  M7 

Uemorrhagp  or  softening  in  puna  ('1431  fslS 

Tumor  in  or  comprcMing  pons  (tr»0).  KW 

lIoniorrnHgc  or  softPDing  in  medulla    (544).  WO 

Tumoi  in  or  mmpr^ssing  medulla  (iKiti).  Ml 

nolulUmus.  '142 


A.-ui.'    t-r    Apoplectiform    l'nli.irtiiT|.haliti»    Superior    (Wer     54S 
iiirkp)    (5S4.  104t!-S). 

Ai-ute  or  .\poplccliform  I'olior-ncophnlitis  Inferior.  Acute  Bui-    B14 
bar  pamlysis  (KM.  Iftlll-Sl. 

Prosre^'ivi"     nphthnlnioplezia.        Polioencephalitis     Superior    M^ 
Chronica    (often   ^ymptoroallc  of    n    Bteadily  proBresaivc, 
moiv  widpspicad  disra>p,  «uch  a*  labes,  tumor,  etc.). 

I'l-o-n-wivp    Iliilliar    Paralysi...        Polioenwpbalili*     Inferior    54ii 
(■|ii>iMit:i.      Kihir-glfwopbaryamal    Panilysis.    (llftt.    T'M. 


commi-nccs  in  thr  small  mnflcl.-s  of  the 
«B  follows  and  i.s  dependent  upon  the 
pnral>-»i».  wilh  ankle-elonus  and  often 
nnd  of  very  chronic  counie.    Mechanic- 


(illCi.  SiHi,   llTiOl. 


Prosressiif  Spinal   Miiocular  Atn^iby.   Amn-Pui-hcnnc  type     MS 
of  muscular  ulrophy.     Chronic  Atrophic  Paralyats.    Chronic 
Poiiomypltlis.     («ei,  soo.  iinni. 

liifnulile.    Kamily,   Ilcrrdilary   Anli-rior   Poliomyplitis  &1sn 

( AV'-iilnig-Hiiffamnii  t,\  pe  I . 


y  of,  or  hemorihajie  la. 


Aoutf   'ir  dironic   mjeliti* 

i:i;iii). 


of.  <-nfi.  R3«.    r>-.o 


be  assodatednith  ntrcpbj  of  the 
paralysln  may  be  due  to  tempnrary  arlr 


mbncKH,  linsling,  feclinc  of  congetrtion,  rcdiicK 
jinptimis.     Pain,  in  Mie  form  "f  a  brn'hial  n'-u- 
■B  of  thr  hand  and  even  of  the  fori'arm. 

iai  "pnsm  in  the  c-ntral  nervoim  system.     Whpn       ArtrrinI  diseaic. 


Piuhynii-ningili"  h>perir«iphica   i-.-rvicnli*.  -wl 

Tumor  ia.  or  ionipr;«.Miig,  is;tll)  '*''- 

SvrinBoinyelia.      CVntral    alio*i«.      MorTan's    Disease,  (tW:i,     Wn 
'M)2.4n-2,  lIKit).  IKi2.  IIT".  lU'T.  i:iin-21. 

M)ii>thc-iiia  travis.     Pseiidoliulhar  Paralysis.  5.%4 

Intrr-niltcnt     Limping    -r    ria.idir.ition       D,*-rf.asia  Angio-     553 

twirioiicn,  (iinni. 

nunily  I'lriodi.-  Pnral.vhi-,  »« 

Prcur-  o(  cpr*ks,l   rit.  M,...n   -ub-claviaa   artery.  53T 


CHART  Xc 

Combined  and  Intermittent  Paralyses 

Comprising  Numbers  471  and  474  on  left  side  of  Chart 
and  535  to  557  on  right  margin 


139 


cr 


DIAGNOSTIC    SYMPTOMS    AND    TB6TS 

( Etilnlirnl         symp-       If  the  parionl  doiM  not  pri>mplly  dip.  one  nr  more  crnnia]  nttyet 

t^mg.  eia   (52."i).    There  hit  usually  iJjsn"    '-     ■-    ■      •       -  -■- 

tomx  at  fint  may  be  more  iinilntenil. 


DIAGNOSTIC   ANALYSIS   OF   SYMPTOMS 

.VeiLti 


ABSTRACT   OF   SYMPTOMS 
There  is  mor'*  or  Ickk  niiirknl  simslje  pnrsplc- 


Craalal     nerve* 
nlone  ItivoIvmI, 
(Pies.  18,  23,  33. 
38.) 


f'rniscij  ptiralXKii 
(2.V!)  and  bulbar 
i.symphonis   (-12'1). 


TaralysiB  of  uiie  or  wore  pye  muirclus  ot  o 


I   of   ficbl    (hntli 


li'lc  mill  of  ano  bdiI  li-^  "f  n|ipiw 
branclii-s)    ot  Irigennmiil  mrie 


( Hiitlm 


syui|itiitii» — 134.)   Symp- 


mill  1(^  of  opposite  sirlc. 


1  ami   |i>5  of  oppi"*ilf  *i'l''. 

i;i'.  i"irk,  rheene.  i-iinned   fmifl.  cic.)    anil  ther^torf  ooriire   in   croups  of  pr>rRors\ 
fm  i-  .«-ii|F)r  r'>f'''r'''f'    Anihl.vfipia,  lilplopin.  ptosis  ani  myilriasis  are  alnnyK  pn 
■iy  llip  motor  rnininl  nui-Iei  are  fonnc]  di^raiwd.  biil  Ihe  apiiinl  nerve  cellfi  n 
I  very  hish    morlalily.    anil    in    due    lo    Ibe    ingestion    of    the     linriHii* 

The  onset  ot  parnlytris  in  sudden.  It  the  patioDi  ilo^s  not  die  prnotptiy,  later  Ilie  syTnplonii<  are  recressive  mther  than  pro- 
grcBuivc.  Tliey  are  iiminlly  nnilnteml.  but  may  lie  liilal«tBl.  A  number  of  motor  cranial  nerves  are  paralysed,  while  there  is 
a  upHstie  |inm1>-!ii!^  more  or  les«  piwnoiinn^  in  (he  arms  and  b'zK.  Verliso  'ia  a  eommon  symplom.  May  hp  due  tn  rurate  in- 
llammalinn,  hemorrhnse,  thrombosis.  omboli>mi,  or  onmpreninn.  May  oef>iir  in  aeiito  antiTior  poliomyelitis.  Often  due  to 
•vphilitic  enilnrteritis  or  syphilitic  neuritis,  or  to  nleotiol  or  other  piiisons. 


raraljuis  of  hyimclosMi.*  <>t  riui'  sidf  an 

A  dijtease  rntiacd  by  i-iilin:;  niii'ili'*!  fnod  (siiiisni;e.  ; 
even  apliaRia.  Tin-  mosl  charaetiriHlie  -j-mptorn  i 
especially  the  exli'rnuf.  are  paralysed.  At  the  mil 
pfltion  it  a  prominent  symptom.     The  diKease  hn\ 


inset,     Regre«»i-e.     No  optic  neuritis.     A  variety  ofapoplexy  (3041,     No  increased  tenmon  of  cerebrospinal  fluid, 
onset.     Progressive  couree.    Optic  neuritiK.    May  be  Jnctrased  len»ion  of  cerebrn.^iinal  fluid, 
onset  and   regressive  course.     .>o  optic  neuritis.     No  increased  tension  of  ce re bro- spinal  fluid, 
ironic  onset  and  progressive  course  and  optic  neuritis.     May  he  increased  tension  ot  cercbro-spinal  fluid. 
r.\rni«  onset  nnd  rcgreseive  course.     No  optic  neuriti!>.     No  iuoreui^ed  tension  of  rerohrc-spinal  fluid. 
[chronic  onset  nnd  progressive  courae  and  optic  neuritis.     May  be  Incrcnsed  tension  of  cerebroipinnl  fluid. 
tc  onset  and  regressive  course.    No  optic  neuritis.    No  incri-nsed  tension  of  ccrebro-^pinal  fluid. 
Chronic  onset  nnd  progressive  course  nnd  optic  neuritis.     May  lie  inoreased  tension  of  eerebro-spinnl  fluid. 


r Annie  ( 
[Ciironic 

I  Chi 


I'ho  ba' 


.■e  eaten  tocpfher.  The  first  ajinploms  are  proalralinn.  nau* 
nd  often  in  an  rilreme  decree.  TTie  pupil  \9  immobile,  i 
involvefl  Hlher  clinically  or  patholngieaHy.     There  isliHli 


I  nnd  vomiline  fnl|on'#d  by  d,vsarthrii)  and  dj'sphai 
[■omm™lfl1i'in  !■  lost  and  one  or  more  of  ibe  rrn-li  mi 
or  no,  mental  diMiirbances  or  fever,  but  obslinnle  < 


weles 


i  more  or  lf«5  pittensive  paralysis  of  the  motor  n 
.  nystagmus,  etc..  may  result. 


"liere  is  paralysis  of  the  tip*,  toneue.  pharynx  and  Inryni 
tlipin  and  dysphagia  and  usually  ataxia  and  respiratnry 


liMiiir    Tti"     chronic     forms    of    these  (The    pnnalysis    in- 

iliiiea>if«,  witli  the  spinal  form    {fi4T-S)  volvca  the  eye  mus- 

(iinsliliile      the     procre«<dve     miisnilnr  HeB, 

alropliieH    and    re)ieinhl(»    the    musndar  j 

dytilrophieB  in    thai    the   pamlyBiB  and  i  Tlie     ])aml,VKis    in- 

(ilrophy    adranee    toEelher   slowly,    nnd  vniviis       the       lips, 

il  ifi  difTiniH  In  «ny  which  is  primary,  tonciie.        pharynx 

Tlier  alxo  eon^litute  a  group  of  rtironie  land  larynx. 
di'Eeflfvntive  atropbiM,     The  paralysiB 
in  purely  motor. 


.V  eradiial  oi)»ei  of  wenknrss  of  onilnr  muscles.  It  may  he  atpndily pmcre'isive  or.  haiing  progressert  to  a  certain  point,  rt  may  remain  Bnitionnry,  Mu'wiles  may  he  altarked  in  any  order,  ptoas,  s<iulnl.  im- 
mohili-  eyelnlN.  inimoliile  p"pil«.  The  disease  may  attnc':  only  thoerfmal  niiisele*  of  the  ejcball  (ophthalmoplegia  external,  or  only  the  inlimnl  mu.^les  (opbibnlmoplesia  inlertia).  or  both,  (ophthalmo- 
pWla  er,mpleial.    Disease  may  be  mmpHciitcd  by  bulbar  paralysis  (Mfil  and  ip  iiaunlly  associated  with  amyotrophio  lateral  sclerosis. 

The  li'ail  il  lirni  f'lnvanl.  Tliore  are  bulbar  symptomK  f-1241.  TTiere  are  dit>olintr  of  saliva,  dysarlhria.  d>'sphnsia.  and  aphoma.  PnralysiR,  Iri-mor.  atrophy,  fibrillary  oiintrnction  of  musele*:  of  tongue.  Iip», 
iiv.il.i.  pharyax.  larynx,  etc.  Roth  facial  nerves  an-  involved  in  so-iie  c.ise=  The  pnrnl.v>,ts  very  slowly  proEresses.  There  are  symptoms  of  a  mild  spastic  parapletria  i"  lei?<  with  ankle-rlomis  and  Babinski. 
A  (llKiaic  at  adv.iuced  life.  Oflen  awodaled  with  ani.vtrophie  lateral  srl"rri;i=  nnd  nt  limes  with  proure^ive  opIiHialuioplegia  (fi4Ji1.  In  nddtiinn  to  tlic  pseudo-biilbnr  paralvsis  of  myasthenia  gravis  (Ttn4) 
ther"  jK  nnrtlier  form  due  to  lesiono  in  both  cerebral  hemispheres  in  which  Ibere  i\  no  muBole  ain.phy.  or  filirillfition.  and  no  chanee  in  (he  eli-ciiieol  reaction,  but  alt  the  other  symptoms  of  bulbar  pat^lysis 
more  or  lew  marli'd.    There  is  more  mental  impairment  and  greater  emotional  excitability  than  in  true  bulbar  parnl.>-sie. 


Kya 
V'-i" 

moirieal 

parnl 

■ing  in 

the 

small 

rmis^le 

of 

hands 

or     in 

Minnlrlpr       C 

irdle 

Spinal       n  e  r  V 
alone  iuvnlveil 
II-'iRi'.      21-7. 


The  niimeles  afTect'^d  *hnw  ppogresBive  weakness,  atrophy,  filirillai 
hand",  nr.  more  rnrelv.  in  the  muscles  of  the  slioulder  idrdle  (aci 
nlr'iph,v.  Tlie  Ihumli  cannot  he  brought  arroso  bnnd  lo  lonch  Ihr 
Ualiinsht.  tmt  nnl  nlwayn.  Tliere  arc  sr'i^ndnr,v  eonlractiirrK.  <"^ii 
»1  irrilaliilily  of  muscles  is  inerenseil.  Rflrn  assoi'ialed  with  p'""' 
inil  eiiliitiins  are  invulvi'il  or  not.     I(  is  diflimlt  to  dra*  any  -iicl 


-Tnie  xyniptomK  as  alxive,  but  s 


r  other,  sympt-ms  of  lateral  sclerosis,    Tliis  .lini- 


las  Ijc 


rar.lcd  a 


n  ehro 


■  polio 


'Oie  two  diseases 


howei 


',  differ  radically  eliologicnlly.  pathologically  and  rlinicnily. 


I  in  the  muRolp*  of 
t]ie  Ibighs  nnd  but- 
toelw. 


tory  1 


tiKC  commences.  In  the  iirsl  nr  second  year  of  life,  with 
V  year".  The  niiiseles  exhihli  ihe  reaction  of  degvnera 
and  willKiut  any  intolvincnl  of  the  pyraiaidnl  tract. 


symmetrical  atrophy  iif  Ibc  muscles  of  the  thichB.  pelvis  and  tiaek  gradually  extending  njiwards  and  downwards,  finally  involnne  the  bulbar  niii 
n  nnd  little,  or  no,  pseudo-hypertrophy.     The  leaiou  consists  in  an  atrophy  of  the  nerve  cells  In  Ihe  anterior  horns  and  a  drgeoralion  in  Ihe  nntei 


Alnrknt  seiiMory 
ipaptomifc  an-  pres- 
ent, Niich  as  pain, 
pnrcsthewiae,  anes- 
llie...ia.  etc,  with 
Ihe    motor    pamly- 


Diwioeiafion  ot  na- 
wition  (Sft-il  1* 
present. 


Holh  armn  and  legN  are  paralysetl.  There 
are  tropbic  distiirhancefi  in  Ihe  arras 
and  nol  in  the  !<■«■.  Pupils  are  often 
une()iinl.  Reflexes  are  abolished  in  the 
arms  and  iaiTi-a*e<l  in  Ihe  legn.  Bab- 
iiiHki  and  nnkle-<<lonus  are  prejieni.  The 
bladder  is  usually  more  or  li*a  dis- 
teadeil  :  ll»  delni«/>r  heinE  paralysn). 
Conlrai-Hire^  may  he  present  in  Ihe  legs. 


litic  iTiyelon 


[,  (Dosl  eitonsive  in  first  few  days  and  t 

.    Symptoms  continue  to  extend  for  s  im 
iialadii    (12in. 

i".  intense  pain  and  spann*  In  arms  and  nei-k  pnuwlc  ih'   i 
1.  in  the  lalcr  slllBe^.  (pnslic  symptoms  appear  in   Ihe  legi 
Mosi  of  thi*c  r-a'fe  are  the  result  of  chronic  s.vphilitie  ni" 


ay  slowly  improve  Inter,    May  be  deformity  in  cervical  region  of  spine.     Knee-jerks  may  be 
lime  and  are  fnlrlv  Kymmetrieal.     Organi""  reflexes  disordered.     A  history  or  otlier  evid-nci 


absent  in  early  ntages,     faimliar  piinctun 
of  sj-philis  (12(^1   is  often  found  in  syplii 


Very  chronic  onset  nnd  a  progrcMive  n 
iri'ilalive,  Intrn-niertullnry  paralytic.  ' 


Fmplni 


mralysin  and  c. 
Culaneniis  en 
ninuilis. 

Sy-mptomK  at  flrvt  mainly  unilateral.  Iie< 


ures  and  musculnr 
;   (herpes,  pemphig 


atroT>hy  in  hands,  "claw  hand."    The  flexor  miisch 
s,  etc)  are  not  uncommon.     Cercbro-spinol  fluid  r 


aie  more  complelely  paralysed  Ihan  Ihe  ex- 
r  he  under  increnseil  tension  and  show  lym- 


;  liilalcral  later,     Ccrohro^ipinal  fluid  may  shn* 


reri'ical  enlarge- 
ment of  spinal 
cord.    (Figs.  M-G,) 


9  ot  % 


■•.  the  mo«t 
Trophic  liuionh  are  usually  pmmir 
Irophie  *vmiitom»  predominate  ove 
pre^iinl  the  t^^-mploms  may  be  both 
geniled  in  e"nlnil  uliosls  in  Ihr-  cervical 
rapid  eeiir«e,  ami  may  exhibit  »  unilate 


•hamcterislir  »j-mptom  and  Is  cunhiricfl  with  luiiii  /'ml  pare^lheniae  and  more  nr  leirn  motor  paralysis  nnd  atrophy.     The  muscular  nirophy  has  often  the  location  and  diarwi-lpriilii-i  of  Ihal  of  proErcMive  «pinal   miiwiilnr  alrot)hy   (EVtSl, 

;il.     Pemphigus,  ulceration  ami  mulilalien  of  ibe  band*  and  trophic  lesions  of  bones,  musclrfi,  nnd  oilier  tiwiiies  occur  in  ihe  lyne  called  Morgan's  disease.    7n  the  most  common    fonn   Ihe  0"riical    reei-in    is  alone   atfeotpil   and   sniBory  and 

molor  syinptmns  in  the  nrm*:    while  ibelw  -bow  a  milil  (.pailic  paraplegia  (TiQTt).  nnd  fN^linsis  or  kypho-ii:  occurs  in  mere  thnti  half  Ihe  rasps.    Paradoxical   (S71H   and  spontaneous  sensations  have  been  mdnl,     When  a  diffuse  clioma  is 

and  legs,  and  Ihe  moHir  sj-inplonia  are  iihoTii  as  prmnincnl  an  the  sensory  nnd  may  be  unililoral  in  Ihe  eariy  stasies.    .VII  forms  of  reflex  action  are  abolished  when  the  cervical  nnd  Inmhiir  cnlnrcemenl*  are  involved,  hut  are  exae- 

dorwil  regionx.    The  ceriical  form  ot  Ihe  ilisi-nit.-  nins  a  chronic  coui-bc.  extending  al  limeji  over  ilr"ar|n>.  Inil  -lowly  pro^roses  nnd  the  anesthesia  at  firat  slighl  sl-a'lily  beconup*  more  mark,r|.     The  dilfuse  form  often  nins  a  fairly 


All   Oie   mu«-W   of    T 
thr  body  and  head. 


111.  ^aslic,  musiiilnr  pnralysi 


agits.     In  such  case);  (he  lesion  comnien''e 


alaru 


cl,.1 


,.««.""'' V'""  "^  *^''  '^^'^'"^  '•  •*"*  ™P'''  •i'^nP  nf  11"-  mnsHes  when  in  aelion,     Paliriil  can  walk  well  at  the  slarl,  but  afd 
artjoa  r.fiHil.    There  i.  no  miisnilnr  atrophy  and  no  rwiction  of  dpzeneration.    In  the  donijiin  of  erulal  nerves  (in  which  the 
■d  an  necnunl  of  the  ptiwis.    TTic  aympinmsare  slieht  in  the  morning  n.tid  grow  worse  during  the  day. 
ilop»y. 


and  nsceiiids,  producing  the  symptoms  simewbal  resembling  a  i 
lation  of  tlie 


i-ry  chronic 


Mi-ending  pnmlysis. 


mlti-i 


rely  of         Rnrrt>   the  di-. 


nl  Ihe 
u-k^  of  pijnfiil  r 


forn  tow  hundred)  steps  ih  tired  out.    The  same  ik  true  of  all  other  volimlnry  acts,     KKaminntion  of  the  nniscles  tvith  eleriririty  ci 
«e  usually  coinmene"*)   there  may  be  ptosis,  diplopia.  O|ilithalmopleuia.  diplegia  facialis,  dysarthria,  dytminesia,  elc.  and  all  the  spinal  nenee 
No  sensory  ^sTuHiaiices  except  painful  cramps.    Organic  reflexes  normal.     A  tumor  is  often  found  in  the  thymus  gland  and  multiple  foci  of  i 


nnislheni'"  re- 

leil.   The  hi-ad 

11  round  cells  (lympho- 


e  cramp,  and  weakness  of  lee  or  lesi, 
r  both  arms.     No  senmiry  diahir'>anei 


»..!  by  V 
•ept   poi 


Ih  marke<l  arlerio-f 
>ciaied  with  apbnsi 


rieriofi  of  leg  as  tihown  by  palpalion  and  by  the  X-r 


Comnienring  in  legs 
extending   to  arm>. 


rate! 


1-  rnuBwl  by  „  cervlfiil  rib,  and  is  often  relieved  by"  olevniio 


e<l  allneks  ot  I 


e  by  motio 


1  decideil  pareins,  which  pa»se-  off  if  Ihe  arm  i.  kept  al  re*t.     .\n 
In  ran?  cases  this  pnrnl.isii,  al  fin.|  intermittcnl,  may  become  [ 


<^ 


DIAGNOSIS 
Hemorrhage    softening  nr  acute   infl.iinmation    ii 

(.■i4:m.  cm  74fH. 

Tumoi'  in  or  coi(ipre«siiig  the  brain-stem  ((idi). 
Hemorrhage  or  softening  in  cnis  cerebri  (543) 
Tumor  In  or  compressing  cnis  cerebri  (flG6), 
llemorrhnge  or  softening  in  pons  (54!1) 
Tumor  in  or  compre.s.sliig  pons  (ff>6), 
llniuormnge  or  softening  in  misliilln   (Thl-l), 
Tiimni  in  or  nimpreKsing  nitslulla   (tkV!). 
Iloliiliiiniuii, 


"f  .-yeball    f.^rd,   'Ith   and   filh)  ;   «n   that    ptnsLs,   aiiuinl.   double 
id  12bh  nerv(«l   with  conse<|iienl  dysni^ 


Vcuie    <,r    .\popleetiform    Tolii 
niekel    (3S1,  iWi-Rl. 


■  or  .VpopIecHform  PoHnen 
-  i.araljsis   (534,  HMCrSl. 


.■iic'phalilis    Superior    (\Ver- 
ephaliiis  Inferior.  .\mte  Bul- 


y  contractions  nnd  all  degrees  of  alteration  in  electrical  «xrftn,hilify  from  simple  dimimilion  to  complete  reoction  of  deseneration.  The  progress  commences  In  the  small  mnacles  of  the 
nulo-h'imeral  type),  is  usually  fairly  s.vmmetrical  o-d  extends  lo  the  other  grmips  of  miisdies  in  arms,  body  nnd  even  Iocs.     The  muscular  wiaknew  fnllon-^  and  is  dependent  upon  the 

lillle  finmir.  The  finsers  cannot  be  spread  apart,  nor  can  their  ln.«tt  two  phnlnnices  he  extended  on  the  (in?l.  The  le^s  shown  ni^ld  di-gree  of  spastic  pnralynls.  with  nnkle-eloniis  and  often 
■eiiillv  til.-  "daw  hnn<t."  Tlie  head  is  usually  bent  forward  \i\i\  [here  is  much  deformity  nlmut  bhe  shoulder  and  other  parls.  A  dixcaee  of  adult  life,  nnd  of  very  chronic  coui^e.  Mechanic- 
.■re^-ivc  hiilhar  p.Tnil,\-si«   (.">4fll.     Some  niithors  divide  this symiiKcm  complex  into  two  grmips  according  a*  to  w-helher  the  atrophy  or  the  pnraljtis  is  primary,  and  as  to  whother  the  lat- 

di"tiavtinn  elinmilly.    'itir  one  fdrin  may  he  an  earlier  sta'.-e  of  ilie  iiilier.     Tile  symplom  complex  is  divided  into  two  groups   (&4S)  in  this  chart. 


i  nnd  lerminnling  fatally  nl    ilie 
r  nerve  roots,  without  inflnrama- 


I'rosrci»i\,'     Ophthalmopleaia.        roUoencephalitis     Superior     bi't 
rhninini    (ofleri  Mymiitomalio  of    a    steadily  progressive. 
mor-  widrspivad  disfO'C.  "nn*  as  tnhes.  luinor,  etc.), 

I'loarvv-ivi.    Itiilbar    rarnlysi«.       Polioencephalitis     Inferior     Mil 
Chreuica.      I.ahlo-gh-s«.pl.nrynKPaI    Paralysis.    HifH,    im. 

n.-.n. 


(mr..  '^Hi.  iirifli. 


Progressive   Spinal   Muscular  Atro|diy,   Aran-Diiehennc  type     T*i^ 
of  muscular  ntrnphy,    rhronic  Atn-phic  Paralysis.    Chronic 
Polioniyelilis.      (6SK'..  «00.  I.IWII. 

Infantile,   li'aiully.   Hereditary   Aulcrior    Puliniujelilis  Msa 

(W-rduig-Hoflmnnn   type). 


Injury  of.  or  hemorrhage  in. 


I'achymininsili*   hiperlrophic 


of.    ITOS.   S3R.     WO 


alk-ins.     rtiirioj;  the  attnck  the  feet  are  cold,  nnd  there  is  ditninished  or  absent  piilsalii.n  in  arteries  of  feet,  awocinteil 
ifiil   cciimp'.     OrEanic  reflex™   normal,     .^mdo-spaxtic  hemiplegia  in  whidi  temporary  allacks  of  hemiplegia,  sometimeu 

7-I"nw  »'?*  Mn'k  "i''*^n."'  '■""  "'"*!!.'''*  "'  ""'  ''''"  """il'y  fi""*  and  then  of  arms,  ladling  a  t"*w  lioum  or  days.     Tlie  allncks  usually  ocnir  in  the  mornini:  cr  after  nil.     Durins  Ihe  atlnck  the  left  cardiac  ventricle  may  become  Icaipororj-  dilats-d  and  a  murmur  may  he  beard.     Tlic  cranial 

in  «em-  ™,.!,.  Ir  f      ■l""'  '-  "'""'''  .     ,'  ™'''<'^  heredity,  or  Ihe  disease  .unirs  in  family  inwups.    During  a  severe  atlnck  there  is  oflen  a  diini ien  or  alienee  of  ihe  i-eflexes  and  of  Ihe  fnnidic  and  galvanic  excilahility  of  t^e  nervcc.  nn.l  of  the  mwhnaicnl  excitability  of  the  mnseles. 

in  «>m    croups  of  family  penod.c  paralysis  these  negative  symplom.  are  not  prescl.     S-m-of  lUe.c  ra«.K  nn.  apparently  due  lo  malari.i  nnd  cm  be  cnr.-l  by  the  admini-l ration  of  qninino. 

ell  and  mn  be  swn  wxlh  the  X-ray,     In  tome  cases  of  rerviml  rib.  atlnck*-  ncrur,  but  nnlv  after  use  of  Ihe  arm      Tliese  niiaikx  >in,  iiKiinllv  nnihiienil.  nrii  ihoiiirb  ibe  erlra    rib  i»  on  both  sides.    The  attack  cnnsisis  i,t  numbnew.  linclini;,  feelinc  of  congwrtion.  rednen*  of 

nili-"!  fracture  of  the  clavicle  will  rarely  cause  similar  «.nnpliiin«.     Pain,  in  Hie  fonn  of  a  brachial  neu- 
Finent  and  may  be  araoolalifl  nith  atrophy  of  the  musdcK  of  the  hand  and  even  of  the  forearm. 


Svringomyelia.      CenirnI    sliosix.      Morvan'*    Disease.     (fiOS,     K« 
S02-4tl-2.  lOon.  nr.2,  1170,  11S7,  1370-21. 


M>asthenin  gravis.     P'.e.iito-hulbiir  Para 


Inierniltlent     l-imping    cr    Clnn.liniti.ni,      Dy»l>aKia     Angio-     5fvi 

si-uroti.-a.  mnn). 


Kamily  Pcriti.tii    l•ar.^ly^i 


Pre«-<ure  of  eerviisil  rib  ii|ion  •iil-chiviau  artery. 


ry  paraly«i 


very  rarely  i 


of  cerebral  onjin  such  parslysej,  are  of  limited  eiten 


net  with  in  hysteria  and  in  elderly  per»ou&  with  thickened  arteries, 
when  of  Bpina),  general.     See  aleo  occupation  neuroses  (615). 


which  CHtJCK  apoplexy  is  prnbntil 


"f  I 


r  paraly: 


i;  may  be  due  lo  temporary  arterial  •■pasr 


rMnlral  ner 


When       Attrrial  disease. 


^ 


CHART  XI 


Convulsions  and  Spasm 


DIAGNOSTIC  ANALYSIS  OF  SYMPTOMS 


Symptom 
Analyzed 


Tests 


370 
CONVULSION 

OR  SPASM 

(242) 


Character 


571 

CLONIC 
mainly  (246) 


572 
TONIC 

mainly  (245) 


r 


Extent 

GENERAL      Diseases  in  which  convulsions  occur  are 
CONVULSION      set  forth  in  Chart  XIa. 


LOCAL 
CLONIC 

SPASM 


f  GENERAL 
TONIC 

SPASM 

I  LOCAL 

TONIC 

L  SPASM 


1 


I  Diseases    in    which    local    clonic    and  all 
>■     forms    of    tonic    spasm    occur    are  set 
forth  in  Chart  Xlb. 


573 
CHOREIFORM 

(272) 

574 

ATHETOID 
(271) 


r 


Diseases    in    which    choreiform    and    athetoid  spasm  occur 
are  set  forth  in  Chart  XIc. 


141 


CHART  XIa 

General  Clonic  Convulsions 


Comprising  Numbers  571  on  left  side  of  Chart 
and  575  to  596  on  right  margin 

Idiopathic  epilepsy — 575 
Symptomatic  epilepsy — 576  to  596 


143 


DIAGXOSTir  SVMI-rnMS  AND  TRST8 


f  Ix«s  of  ponscious- 
I  oeee,  (comn  or 
iii>ini'<-i^ma)  (SK). 
Krwiiipnlly  hiliDB 
ft  till-  toncup  or 
nllirr  iDJury.  Short 
I  itiiriitiuD. 


No  other  ajiDptom 
of  dtspaee  except 
tbe  coDvolsion. 


SfmptomE  of  seri- 
ous brain  dUeaec. 


DIAGNOSTIC   ANALYSIS   OF   SYMPTOMS 

ABSTRACT   OF   SYMPTOMS 

ntlnrk  flo  erjinil  mnt).  is  nt  first  tonic  with  ■irr.-.i  .,i  T.^im  ,,ti..ii.     Thr  fnc 
'Imiie  ipiKon  of  lonj::(>r  liiirntion    (J  to  5  rnitini.  ■  i    uhi [■^y,    rPH|iiruliot 


,rlinll<i  nml  nyWciniis.    Al  Iimi-s  nrinr  nnii  fi 
>'li.f,v.  ptc.)  i-iilhHl  tlip  "ai'nMiry  iiiini"  t'l2n)  .nnrl  j-  ..frr  u  u-ii,  i 
.niiilly  ahsent  Hiiring  anil  inimwlinli'ly  ofirr  thr  artjuk.     A  .I.i- 
in  (III  llii"  fordieail  and  fiioo.     C'lmiplpti-  nmni'sin    in  rtennl  I 
any  p^m  <'f  thr  hoiJy,     In  som"  ra-^os  Ihf  iitiiickfl  oiv-uroiily  at  iiicht  or 
It  nirtliiil.     At  limes  Ihi-re  in  mircly  loss  of  pnnsi'iousnct  wiihr.nr  h.'Ii.i 
lund  lepil<i>sin  iii'rx'iirsivn  rotntorin)   or  piTformK  a  siii^-  ■■(  vis   ■  ■  m 
itin.k  of  Aoitr  fo)l"W(i  or  ri>plncpH  h  i?ouviiliivc  atiaok   ([isychic  (H|iiii  ili  m  i     In  . M 
pillcDts  mo  iiMinlly  rfull  and  aliiptd,  nfton  finstnirtivr -iml  .i(i|.,iMrii  I. 
pblcn-Blifin,  by  the  purposeful  and  linx-ly  nnliirc  of  (he  Mttioli.  I: 


mmtial. 
made  hy  li 


A  oonvuUiv(>|(aek.  r*ip< 
not   repr-ftl 
irritation 


[The        conniliion 

Ihf  miwdM  flt 
Htmul  Ihi-  wiroo 
time  (epileptiform 
( coni-ulsion). 


Congenitol  or  in 
infancy.  Often 
ferer  at  onset  of 
first   convulsion. 


Till'  disi'o*(>     onpnil: 


tempo  n  I 


steadily 
usually 
toms. 


nckf.   which   arc 

noahu'we  of  tbe 

•  syiuptomB  of  a 

nt^ttg    brntn    diBeas^   n-ith 

Wiuory  and  psyWilc  x.iTitp- 

rl«ady    advance    towards 


Symptom B   of   dlH- 
rase        of        other 


of  cerebro-spinal  disease, 
r  Kidney  disease. 


thni 


the 


Cardiac  d 

'  Blood  dim 


InlcntiOD  Ir  r,  iconninL;  speech,  nystagmus. 


and  tb<> 

Slow'  pul'P 

nupid  U-i-t 
dilation 


Symptoms    ot    poi- 
soning. 

Appan-nt.  but  no  true,  coma  (shown  by 
RiiKcplibiiliy  to  etiBt'ention  durine  Ibr 
altnek).  No  biting  of  tongue  or  other 
injury,     l.oni;  duration. 


(■Blue  line  on  Rums,  lead  in  urin. 

1  .Mrohnlic  odtir  of  hrenlh  and  iti'Ti*   inmot  and  ncrvousne 
I'k     irars  in 


itendy  gait,  motor  sod  sensory  paralysis,  many  symptoms  of  I"cbI  lesion^,  etc. 

of  convulsions,  accelerated  respiratioo.  restlessness,  cyiinosis  and  cotiimctt<d  pupils.    Oflen  edema  of  lungs  and  of  other  liwut-      The  urterinl  tension  i> 
contains  albumen  and  many  casts  and  is  usually  scanty.    There  may  be  albuminuric  retinitis,  hexdache,  vumitinp,  Cheyn^Siokes  rc.iiinitlon  and  somnolence, 

B£  iDlermiitsion  in  heart  beats  associated  with  coma  aud  conviilKioos.  which  pass  off  after  the  heart  begins  beating  again.     Arteries  atheromatous.     Advanced  life  usu 

•mall  volume.     Iri<iillicifnt  nmouni  of  blood  or  of  reil  cells  and  hetnoeiubin.     Pallor,  dj'spnoea  on  eiertion  and  strabitimus  are  optiirii'<n.     Often  severp  digestii 
Oflen  the  rciiilt  of  one  large  or  of  repeated  hemurrbagos. 

takinp  li.I.     Wrist-drop.     History  of  lead  colic  and  exposure  to  Icjid. 

Muscular  tendcrneiw.     History  of  a 


ir  i-onvtilaion  alwoya  commenees  in  one 
proiip    of    muscle*    anrt    later    extends 
over  the  whole  or  part  of  one  side  of 
the  body  and  often  over  both  side*, 
(jnoksoniaii  epilepsy  (4211. 


Symptoms  ot  hys- 
teria (4iril.  Sueb 
attacks  have  lipen 
called  hystcro-epi- 
lepsy. 

If  the  conriiliion  remain*  unilnti'nil.  con- 
H'iotisneM  may  or  may  not  be  lost, 
n«iia1ly  not.  but  it  is  aluays  tost  when 
the  c<invnUion  h»comes  bilateral 


Comji  diirins  and  after  the  r 


of     aerioiin 

disease. 

always. 


Occii 


Epileptiform     con- 
ulsion. 
'nmn    durine    antl 


Hendnclie.  hneknch''  and  radiating  pains, 
delirium,  vertigo  and  vomiting,  espe- 
cially on  rhange  ot  posture,  bjfperalgo. 
sia  (vpinal  and  el»ewhorel,  photophohln, 
etc.,  are  early  symplnms,  Itctraction 
of  bead.  npUtbotono«.  Pie.  (2flril,  Pa- 
ralyis  of  cranial  nerves  (squint,  etc.), 
■■ulnncnus  erupt  Inns  (berpenl.  Iftcbes 
I'^'rChralps  and  Kemig'n  KyTnptom(S201 
Tonic  spasm  and  paralysis  arc  mon 
common  In  basal  in6nmmations,  and 
rlniiic  ipasm  in  cortical  inHammations, 


Lumbar  puncliin-  civca 
bloody     or     purulent. 


a  clear  oi 
fluid,     II 
ntniniuB 
po  I  j-inor  ph  0  n  I  icl  e  II 


l.iimhnr  puncture  gives  a  clear  fluiQ 
Increnscl   tcnuion  and  ccnlaini 
ulin    nnil    many    mononiiclenr 
cytps.    and    if    the    diseaac    li 
polymorphonuclear  leueocylcn. 

t.nmhar  puncture  gives  a  clear  fii 
increnaed  tension,  but  no  im 
cellular  elements. 


^      f  .May  occur  In  childre 
I  Coma    during    Ite  J 
I  eonvuUion.  [  Is  the  reault  ol  »om 


al  the  onsPl  of  any  iutceli 
uniiMinl  metnlMiliL-  cbnngpii 


ease,  especially  i 
1  Ibc  body,  and 


nt  first  pale,  soon  becomes  flushed  and  cyanoti. 
iition,  and  froth  on  lips  often  bloody  from  the  tonaui' 
ittai'k.  Thf  attack  is  oflen  precedM  by  twitching  -if 
cry.  "tbe  epileptic  cry,"  In  some  nttncbH  the  tempi-r 
I  Koine  niu4ciilai  and  s'-naory  wcaknes*  (stugi' of  exhi 
^  r.illiAv  an  altnek.  There  are  recurrence*  nt  v.-iryina 
II.  by  iliy  (nocturnal  cpijppsyt.  Tbe  attacks  van  gr 
''■luit'  Qiiloumiic  act :  tlic  minor  attack  (le  petit  mall. 
(automatism).     At  times  the  patieni  is  iinc«nsi'l<i 


liug  rfii 


■  ■I  I  pdepsy  and  in  thnxe  in  nhich  the  attacks  ar 

Malinsercrs  have  been  known   to  imitate  an 

"thcr  evidences  of  consdous  effort  and  by  the  i 


Thf  pupil  i*  dilated  and  inactive.  This  tonic  state  i»  i^ulckly 
whteJi  is  often  bitten  during  the  attack.  TbTe  is  often  lateral  de- 
rortaln  rausiles.  "inoior  aiim,"  or  by  a  sensorv  hnllucinnlion  (lac- 
iiiire  of  the  body  is  raided  and  nlbiuiiiniiriii  is  frequent.  The 
iMtion)  often  follows  llie  attack.  After  a  violent  attack  purpuric 
intervals,  but  attacks  can  neither  be  brought  on  mir  iirfc«lcd  by 
iilly  in  character.  .\t  times  thert"  is  merely  rii;idity  without  doote 
At  limes  the  p.itient  is  unconmiuis  and  runo  (onvards  and  liirni 

and  performs  an  aoi  of  violence  ((-pilcptic  mnnin).    Al  ti 


Idiopathic    Eplb'iisy    (including 
the    minor    attack,    epilcpsii 


very  lre<iuei>t  there  is  more  or  less  mcntui  impairment  (epile|itic  dc- 
ipllcptir  etinvnision  cloiiely.  The  diatsnosis  of  malingering  can  only  be 
onfci'ioii  of  Tnalingcrcr. 


■inllv  common  in  syphilitic  and  rachitic  diildrc 


often  p"" 


,  associal<<d  with  monoplegia,  hemiplegia  or  diplegia,  i 


-bcmiptesic  motor  dlsturlmnces:  ntlictosjs,  rigidity  and  contractures.     Kreqiicntly  there  is  more  or  lew  complete  arrest  of  dptelopmcnt,  physical  and  menial, 
of  epileptic  idiocy  belong  to  Ibis  class,  even  though  they  present  no  paralysis. 


>usiderablc    mental    impairment.      There    is    usually    dy-»arthria. 


HeadnHie,  vertigo  and  vomiting.     Cbokeil  disc  or  optic  neuritis.     More  or 
loss  of  raemor.v.     Iioivilixing  symptoms  are  sometimes  present.     Convtilsi 

Loss  of  will  power,  restlessness.  dcliiKions  (usually  of  exaltation)  and  symptoms  of  Inianity.  Poor  jiidgnieni.  Good  nnturctl  but  Irascible.  Childish.  Characl eristic  blurred 
speech,  TrcmiT  of  loner  facia]  miiscU'«.  lips,  tongue  and  band!<.  and  awkn-ardncAs  (ataxia  and  apraxia).  rncqunl  and  irreaul.ir  pupils,  Are^'ll-'toberlson  pupil,  optic 
neiiri(i<i  or  atrophy.     History  of  syphilis.    Lumbar  puncture  shows  lymphocytosis,  in  cpfobrn-spinnl  lluid,  slibulin  and  a  positive  Wnssemiann  reaction   {412-:11 . 


Illy. 

<•   disorders   \ 


abuse.     Convulsions,  similar  to  the  alcoholic,  not  infreipiently  follow  the  excessive  use  of  narcotic  drugs. 


e  is  always  a  warning  in  tbe  form  of  slobiis  hystericus,  palpitation,  etc. 
ry  irregular  and  violent  and  mnny  of  the  movements  seem  pun'oeefiil  and  to  he  theatrical  posini;  (crucifixion,  etc)  and  as-iimc'l 
illy  lasts  a  Icug  time,  especially  if  the  audience  he  excited.     V.yps  are  usually  closed,  and  the  eyeballs  turn  upwards  if  the  eyelii 
praorbital  nerves,  etc..  especially  if  tbe  audience  be  sent  from  tbe  room.     Moderate  pressure  upon  these  parte  may  cause  an  nlta< 
*tin\  iiymptoms  |4iri).    Abundant  limpid  urine  after  the  attack,  but  urine  and  feces  are  never  passed  involuntarily  during  an  attack,     1 


lUjf  The  convulsion  often  commences  witl 
aiiia.  It  spreads  lirst  throuch  tbi 
order  from  fat 


motor  ftnitchiiig^,  randy  with  a  sensory  (linglingl. 
lolc  ot  til"  part  first  nltaekt<d  and  then  in  a  definite  | 
a.  or  from  arm  In  leg  or  face,  or  from  leg  to  arm.  acconlln;  to  the  | 
unatomical  arrangement  of  the  eorti<'Hl  motor  ceiiier.*;  hence  never  from  leg  to  face  withoutl 
the  arm  being  involved.  The  convulsion  is  followed  hy  a  hemiplegia,  sometimes  transient, 
-ometimes  permanent  aud  progressive.  There  may  be  muscular  rigidity  in  the  Intervals  be- 1 
tiveen  the  convulsive  attacks. 


ifttr  <■! 


B  such  as  headacjie, 


rarely  ihe  pneuuioi'occii 


prodromal  sympb 

'■rBy  lumbar  puncture.  Weichseiha urn's  diplococcus  almost  always,  oi 

I"      selb'ium's  diploeocdiB).    Strong  retraction  of  head. 

"it 

)-(By  lumbar  puncture,  p.^ogenic  bacteria  may  tic  found  in  the  cerebrospinal  (luid,     Suppurntit.n  or  nr 

(tnuues,  carbuncle  or  erjsipelas  of  bead  or  neck,     Uetraetion  of  head  may  be  lew  marked. 

puncture  tubercle  hnciiti  miij  be  fuuud  in  the  cerehro-<ipinnl  Huid. 

choroid  liibercl.'s  may  nn-aKion/itly   Up  seen  b.v  O|>hlhalmosi'opic  exam 


eicposed  to  high  tcmpcrnttirea.     D?liriitm 
•r  other  germ*,  may  be  found  lu  the  cerehr 


■  usually  present. 

i-«pinal  fluid.   There  is  often  an  epidemic  of  the  disease  (Welch- 


|Hly   relievrti   by  the 


uiii  ''inf  Uie  nervous  «y^.tem. 

<•*  ialeitiual  putrefaction  and  other 


if  Moi  all.  of  the  ger 


stion  of  laiulcd  meat  and  other  poise 


^  and  are  not  to  constant  as  In 


diarrhoea  nod  foul  s 


DIAGNOSIS 


■    major  attack. 


■iirring  ahn  in  ndults,  especially  in  pregnancy,  altogether  similar  (epileptifnrml  to  the  ahoic,  but  o<'curring  only  once,  or  in  one  series,  and 
ABOcialed  often  with  digestive  disturbances  and  abdominal  distention  aud  may  be  due  to  poisoning  (ptomaine,  alcohol,  etc.),  or  U>  tli-  Mntvs  lymphaticus.  Slay  be  due  in  some  children  to  peripheral 
Bl  Ihe  onset  of  an  acute  infection.     No  sharp  line  can  be  dravvn  Dolween  llicse  conxiilsions  and  those  of  uremia   (587),  or  lead   (oS4».  or  alirohol    (OSTi),  or  nulo-intoxicatioa    (506), 

r  begins  in  early  infancy,     rnilateral  or  hilatcrnl  convi 


The  shape  and  site  of  the  akuH 


cpili-iisy.    e|.iif|no-    ii 
|i«vchic  [Hiiiivaleiit.  e| 

1  i.-.a. -lii).  ^4:l.  niJs. 


■pil.pl 
7a-s:i,  1101), 


•erel.nil  Pal-«v  of  niiMbno-l, 
(.-.111,  IVJI.  S()L  lt>.->l-SSl. 


Cerebral  Tumor  lineludllig  abneewi  and  cystl   not 

in  or  n«ir  motor  aren  of  MPtei    (507-3r.-7-fl-41. 

:i'*7.  S3C.  ftM). 
ParesU.      Itcnerat    l*«ne«is.      Panilyiic    llemenlla, 

(1.1-..  ISO,  400-12-3.  «7o.  im.  8!i7.   1052.   llOfi. 

ll'ID.  U'ilOI. 

liiv.emlnal<-d   Sclero.i-. 

(loO.  f.n.  o-'A  (itw.  OSS,  "raft.  "os.  -sos.  om. 

IIKMI, 
Iremic  eonvuUion.  (103.  r.7"!,  W-H.  W71- 

.^tokesAdnmi.'   Diaense.    14241,    imKM. 
Amniic  coonilsion. 

Lead  convulsion.   (404.  57(5,  lt>5:n. 

Alcoholic  and   Narcotic  convulsion.    (.17(1.  ll.'iR,  iMB. 


Patient  may  fall  or  glide  to  the  ground  but  does  not  hurt  herself, 
itiitudi's,  (altitudes  pamionellcsl ,  Patients  often  "rave'*  during 
!>  are  force<l  open,  .\tlack  can  u*uatly  be  arredttd  hy  pre!i»ure 
k.  Great  variety  of  sensory  symptems.  Ane*the«Ia  is  usually 
he  reflexes  are  not  abolished  during  the  attack  nis  rony  occur  In 


nulslnn.    (112.   120.    ISI,    l.M.    1S2.    .iSIl 


Occurs  In  youth  and  middle  age  and  often  after  Iraumali^m  of  old  dale.     Headache,  vertigo  an 

iting.  ITsiiHlly  choked  disc  or  optic  neuritis.  Synptom-i  steadily  progressive.  Similar  attacks  with- 
out choked  disc  may  occur  In  Incallied  mcniu^itU  or  other  irritative  lesions  in  Ihe  cerebral  eortex. 

ccurs  in  old  age  and  oflen  after  recent  injury.  A'coholisra.  nthermatous  arteries  and  inianily  are 
common.  Sudden  apoplectic  attack  with  Improvement  later.  No  choked  disf.  Symptom'  pn^ 
Brr«s  paroxy*mulI.v.  and  after  each  paroxysm   ibere  is  m;irk.-<l  improvement. 


Cerebrnl  Tiiruor  (including  nhscew  and  o«tl   in  or 
f  area  of  cortex.     Jacksontnn  Epilepsy. 


(421.  r.07-"*.  IJ02),     (Fip'.  i.viin. 

'lemorrbage  in  or  neap  motor  area  of  cortex  (pachy-    ."iSS 
mrninxilis.  elcl.     Jnchsonian  Rpllcpsy. 
(.-02.  lOTv-^l.     (Fig*.  I.VlCt. 

;,in.ln.kc  or  lleolilroke.  (fKlS.  1070).  r.?!! 

■o-spinal    MeninciHs.   ll«S.    1214,,  r>fln  M)l 


122<l) , 
Purulei 


ingitis,  (12271. 


r  pnrl  of  the  body.     Orindinc  ol  leelb  and  hj-drocepbalic  cry.     Choked       Tubei 


.Serous  Mcniiigilia 
(1241). 


Aiito-loi,ii  convitUion,  (r,7i!.  IWvl). 


(110.123.14'^. 
167.  170.  ISG, 
508.  605,  1045), 


CHART  Xlb 

Clonic  or  Tonic  Spasm 


Comprising  Numbers  571  (continued)  and  572  on  left  side  of  Chart 
and  597  to  621  on  right  margin 


(Note) — Many  of  the  spasms,  especially  the  tonic  spasms,  are  associated  with 
pain,  and  are  then  called  "cramps." 


145 


r^ 


DIAGNOSTIC    SYMPTOMS    AND    TESTS 
Pj'iviin  ID  vi-rr         }iliuL-k-iihc   niuiMiiii  ^llIlita^   to    that    pro- 


acuie   COM*. 


a  dectrJc  shock. 
fOtviir* 


»iugli' 


>   or   Difloy 
timi-«  rvpcntwl 

HliHsm,  rarv'Ir  om- 
Irncliiri',      of     one 

croup  of  iiiii»c1p», 
opciirrinc  in  pan>x- 
yKili*  wbirh  ratlirr 
tend  to  viibsiile  on 
voluntary  move- 
uii'dIk.  MyiH'Ionua 
(270). 


n^KiD!  Id  oni-  linn  an.I  m.Ip  of  n.'i-k  aoiJ  rt"""!*  '"  '^?  "'  ^'^'' 
siili-  uod  then  to  opposite  side. 

nore  rarely  in  neok  ■I'he  siiusms  ar^tlaw'  "'ways  unibteral. 
and  when  bilntwaUre  not  ayiBmelncal. 
Tlier  interf.(t  ntj  HtHe  with  volun- 
tary muvfmeaU. 


DIAGNOSTIC   ANALYSIS   OF   SYMPTOMS 
.\BSTRACT    OF   SYMPTOMS 
Much  pnin  in  hiad  ^iml  iivck  al  ousol.      Wnikfipss  sL.wly   folloi 
oome  \ioipiit  and  ni'Tp  eouiiniiouH.     t^ileptiform  iitlncks  nr 

Tile  spasms  seem  likp  uiimir  eeslures  and 

apneas  to  be  rather  purpoacful-     May      Psji-liie    disHinifrs 
have    ori^'nat^d    from    local    irritation,  Deunistlienic  ual 

hut  have  fieraiated  after  the  irritation 


f    an    emotional 
e  often  present. 


fThe 
1       <B16) 


ItK^iu.'  in  arms  and  may  eiiend  to  lep. 
but  iilmoit  never  to  taoe.  Often  ihe 
tendons  piny  as  in  atihKultu>i  (endinum. 
Symploins  sliow  considerable  variation 
in  different  cases.  In  rare  oikik  there 
may  be  iofeclinn,  fever  and  delirium 
(Hunt). 

BociDn  in  side  of  face  or  in  one  arm  or 
Ipit  and  may  e«tend  over  one,  or  even 
hntli  sides  of  body. 


The  spasms  are  billttral  iind  fairly  »ym- 
njetrirul.  but  not  (jnchronous.  They 
are  irre^ihir  In  totf  nnd  rhyliim.  and 
are      almost    llwiys     limited     to     on.- 


>sed. 

>ipa>nus  never  appear  to  be  purpose- 
il  .No  mitvement  renullr^.  merely  indi- 
dual  muscles  «princ  forth  in  slronK 
intniclion.     Irritation  of  Ibe  ekin  or 

ti'lons  rniiseK  paroxysms. 


I.itlle  or  no  emotional  di-tturbanecs. 
TretDblinc  of  tnusdes  belneen  Ihe 
pnroiysms.  The  spasms  bec«oie  less, 
or  entirely  cease,  during  sleep.  Re- 
flexes exaggeratdl. 


of  mufclrt  and  los*  of  faradio  exeitability.     The  spasms  be- 
'    arr    accomp'injeit    hy    no    pain.      See    also    reflex    spasm 

The  contractures  art  nfiyxTipariir-d  hy  sharp  dirts  of  pain. 

The  muscles  [nvoKed  arc  attached  by  one  end  to  tbe  trunk  of  the  body. 
Muscles  of  Ihe  fn^e,  hand  and  forearm,  foot  and  lower  legs  almost  never 
involved.     No  "lerediiv.     A  dlsentc  of  ndult  life. 


Many  casea  orcur  in  the  satiie  gencralion  of  a  family.  The  disease  beisins  i 
early  life  and  is  aR>oaated  with  epilppsiy  and  dempniia. 


hy  lyinf;  a  hand  (i!.')illy  nt 
li-ly;    bnt  usually  porHism 


iaer-nt  niu.Hcle*  and  so  ovei 
r  many  audi  local  qpaiims.  i 
mud  the  extremity  as  soon 
tvhi-n  Kpat^m  ix  limited  to  ( 


one  half  Ihe  body  and  then  p.is-'<  acn 
IP  may  occur  which  will  pus*  into  a 
IB  tbe  local  ttpasm  nprii'ars.     f'ansriin 
c-hnlf  the  body  or  to  one  extremity. 


ing  in  pharynx 
oenophnru*. 


Rleiilily  vf  aplnt 
CerBlmllar      nia 


There  is  the  history  of  an  jnfi-cird  wound,  or  septie  childbirth. wllliin  n  month,  unually  within  two  weeks.  The  iiifectinn  may  oo-ur  llirouith  the  navel  in  new  horn  b.ihies   fleinnns  neonatorum) 
jaws,  oecitrring  in  pnroxj-jiins;  also  riKidity  nf  facial  mmdai  priwlunnc  "risiis  sartlouiniB."  In  the  onset  a  cradually  increasins  stiffness  nf  masticnlory  nnd  other  muscles  followed  and  ncii 
hclnit  held  in  position  of  opisthotonos,  omprosthotonox,  ptmrMtliolonos  or  ortholonos  (2'S).    The  spasms  are  associated  with  profuse  mealing.    There  are  no  meulnl  symptoms  nnd  no  co'iia, 
very  hich,    The  diacnie  vartc-  greatly  in  intensity.     The  ICD|tr  the  inmliation  p^'riui)  ihc  milder  Ihe  disease.     Ixica!  tetanus  ind  head  lelaniis  with  local  paralysis  have  been  deecribed. 

There  in  a  history  of  a  bite  hy  an  animal  (usually  dog  or  cat)  within  a  year,  usually  within  six  months.    Tin*  most  sirikint:  failures  are  irL-mor,  rapid  pulse,  fever,  mental  depression,  fri^^ht.  \\"r 
especially  on  MBhl  of  water.     Spasmodic  closure  of  phtlTOX  find  oeuiphnmis,  mukini;  swallowinit.  enppeinlly  of  fluids,  imp  >"sil>le.     Saliva  cannot  he  swallowed  and  is  expelled  from  the  m*" 
couch,  opisthotonos  and  genfral  spasms  are  common.     Cefl'l  i"l^  froin  ciitaneoua  or  speiial  sensory  wurfnees  are  creatly  i-icrcased,     especially     lh.it    of    inspiratory    d.vspnoen.      Priapisri  -i"! 
liahl  nnd  aecnnimndalion.    Tlie  since  of  exciliment  is  at  timn  f''ll'Wcd  hy  B  slace  of  paralysis  and  is  often  preceded  by  a  p-odromal  stnee  of  malaise  and  of  pains,  especially  in  Ihe  scar.    Hysn 
noi-is  must  he  made  in  such  i-ases  by  the  preience  of  hydailctl  -yinptoms  (425),  absence  of  fever,  absence  of  true  rcspirnliry  spa^m,  and  by  time. 


'  both  sides,  or  it  may  remain  a  local  spasm  and  pass 
<ir<n.  A  general  convulsion  cjin  sometimes  he  averted 
s  lost  nhcn  the  coavulsion  cxtcods  to  botti  xide«  of  tbe 


Thi-  cliaracieristic  symptom   is  ricid  spasmodic  closure  of 

impnnlcrl  by    paroxyums   of  painful    Ionic   spamns;     the  body 

Totviirds   Ihe  fatal   temiination  the  temperature  becomes 

ir    and   extraordinary    emotional    eseltement,    even    ranuta, 

h    «-ilh  dlHiciilly.     Spasm  of  muscles  of  respiration,  hie- 

Lilly  ownirs.     The  pupils  are  dilated  and  res-pond  to 

penions  at  times  simulate  hydrophobia.     Tlio  diag- 


DIAGNOSIS 
Pubini'i  Disease  or  Klcctrical  fhonn    (62.?). 

Ckmvulsive    Tic     (hlenhnrospnum.    lorticollis,    etc 
(3tt7.  270.  615-B.  726). 


Tic  Doulour-nx  Oi",  T2fJ,  W8). 
FririJreich  b  Paramyoelonuh   Multiph'i 


Unverrichl'B   Family  Alyoclonus  Kpibpticus. 
Jncksnninn  Ri'ileppy  (421.  .V*7-S,  ISOi-.".-!!). 


IS  distiirliantft  or  V'^  of  consciouanejis.     Tonic  retraction  of  neck.  opiKlboloiios  and  hoal-sbnped  retraction  of  abdomen.     Slight  irritation  will  cause  spasm.     Hendachi-,  hackai 
shows  incrllM  of  cells  ill  cerebro-spiual  fluid,  except  in  serous  lueningili.i.     For  different  varieties  see  500-4. 


May  foltott  injury.  Blood  i 


cerebro-spinal  fluid  oblainod  by  lumtwr  pimeture, 

«el.  tbe  far 


1  in  hack.    Girdle  and  radiating  pains.    Transient. 


L'  as  the  lewon  are  addueled,  on  the  opp'.f 
Other  symptoms  of  cerebellar  disease. 


>ide  abducted. 


>r  uo.  paralys 
Head,  trunk 


e,     Exagcerated  reflexes.     Little,  or  no,  fever. 

ind  extremities  each  rotate  about  lone  axio  from  li'le  of  l< 


1  tc  the  -ipposite  side  nnil   tbf  eyes 


Riifidlty  ratlier  Hinn  Kpaxm,  not  slroiig 
enoiieh  le  pn'venl  paiaivv  or  voluntary 
movem^nls   f2«i). 


Apyrexla.      If    nn-| 
Fonn-louRten    la '  „ 
pr«-nl.  see  aloo^  _",".".'!'„" 
epilepsia      media  I 
(57.-.). 


RxlTrmitio  and   trunk  remaii 
\»t.\  minutes,  hours  or  days. 


Rilidily  of 
the  action 


(.Retracliun  of  ti«  hud  and  opistholonos.  flexion  of  elbows,  supination  of  hands,  extension  of  legs  with  pointing  of  loes.     Other  symptoms  of  cerebellar  disease. 

tKf  potiliun  in  which  they  may  be  plncnl  for  a  surprisingly  lona  linie.    Wax-like  resistance  to  passive  motion.     Diflirult  positions  nialniM 
illiuln,  abolition  of  reflexes,  and  more  or  less  complete  apparent  loss  of  consciousness  are  usual  symptoms.     Other  bysterieni  sj-mplom'^ 

fii(v.  meech    monotonous,  passive  tremor  of  hands  and  less,  ciharoctcristlc  altitude,  festinnling  gait.    Tendency  to  full  backwards  or  forv 


ndefinitely  without  apparent  effort.    The  attack  may 
ifien  present,   (451).     See  also  epidemic  encephalitis 


continue*),  to 
escape  altogether 


miiteleK  of  (he  faee  usually  escape  altogether.     Marki4  h' 
IV  Tiiarki'it  hjTHTlmpby,     nosely  allied  to  this  dlM'ast  i«  "| 
insure  In  ciitd  with  eonsefluent  reflex  vaso-molur  spo"^  anl 
■ailed  acfiiiircd  form,  "myotonia  aei]uisila,'"  is  prolmhlj  iv\ 


n  firtt  (ii«vi-ni.-nt  rifti-p  n  ri-xt  or  when  action  Is  done  faster.     I'atie-it  cannot  hurry  or  eJtccute  rapid  movements.     Is  liable  to  li 

ilitv       Mil  iii.ii.    I  ii-.-trical  reaction    (400).     Increasml  mechnn'til  excitability  of  muBclc.  even  slight  prowure  with  tbe  finger-tin 

MIC  iMn.  I  iij -iiiti"    fKulenhere's  disease)   also  on  an  hceditary  basis  (it  has  attacked  twenty-eight  members  of  a  family 

tiiiiiiiii'    iii-iiii!.. cs  in  Ihe  muscles.     A  myotonia  congenita  •niermillens  and  a  myotonia  congenita  atrophica  have  been  d^se 

iilhiji'tli.  ]'  ililli-ii'iit  disca-ie. 

:■  possible 


Ms  (077).     See  also  Encephalitis  letliargiea  (1047). 

enuiljbrium  The  arms  are  le«ui  alTi-clnl  Ihan  Ihe  leu'i  and 
■aui--.  a  idii&gish,  long  eontinutsl  contractinn.  Muscle  fiber> 
in  •ix  gcneralionsK  hut  these  paroxy3iuil  altaeks  follow 
iheil  with   the  rtiantclerislii-s  implied  in  Iheir  names,     The 


of  opistholonoH  (205),     Periods  of  intcrniission  with  relaxed  muscles  lasting  several  minutes.     Cutaneous  and  tendon 
fnnvulftions,  mental  defect  and  partial  arrest  of  BTowth.  are  common.    The  contracture  and  motor  paralysis  may  be  unilateral  n 


reflexes  increased, 
bilateral. 


History  or  evidence  of  ttrychni 


Tetanus  (172).  Tetanus  tmumalicui.  Tetani 
rheuinalictis.  Tetanus  puerpetnliii,  Telani 
ui'onatorum. 

Rabies,     Ilytropbohia.     I.yssa    (173). 


llematorrhaclils  (52.1.  07.^1. 

Lesion  of  cerebellar  hemispheres,     Cerubellar  fits 
fiMT,  fi8fi,  7P3-*,  lOlfi,  I2nfi). 

Le.'^ion  of  vermis  of  c>>rcbellijm.    Cerebellar  fit- 

{Ml.  GSfi.  78.1-4,  lOlfi.  12iK). 
Catalepsy    (10(18). 


Paral^is  Aftiinns.     Parkinson's  disease 

(20-1.  U77.  709.  804). 
Myntnnia   Congenita.     Thom»en*»  dii>catp    (li)il. 

2iki.  Ilfi71.  including  Pammyolonin  Congenita 

(Culenberg's  diseaae). 


Spavm  mainly  con-       Rilaternl  painful  Ionic  spasm  of  muscles  of  hands  and  someUinet  of  feel,  latrtinp  minules.  hours,  or  rarely  days.     Hands  and  fc  I  drawn  inlo  smallest  voUime  possible  with  hollow  deepened   (obilptrical  hand).    Joints  of  arrat  flexed,  those  of  legs  extended, 
fined  In  bands  and  Inereaserl  mechanical    (Trouweau's  phenomenon— 140)  ana  olfelricnl  (Erb's  sign— 142)  excitability  of  nerves.     Facial  nerve  *i'py  irrilable:  so  that  slight  blows  on  it  cause  spasm  of  facial    miiBi).*    (Chvostek's    sign — 141),      Usually    associated    with 

feet,  paroxyomal.  rii'keiii  or  dfcrsiite  iliwrder^  and  intestinal  paniHle*.  or  dlln'oil  stomach:    often  foMows  extirpation  of  panilhyroid  glands.    Sometimes  occurs  as  a  symptom  of  hydrocephalua.  cerebral  tumor  or  other  serious  brain  dispaw  in  rbildren.     It  oecure  in 

iafi-ctiouB  diseases,  in  poisoning  and  in  pregnancy  and  u  u  occupation  neiiniHis   (rtlG).    This  disenae  is  probably  due  esi-ntially  to  destruction  of  the  parathyroid  glands  nnd  may  perhaps  be  cured  hy  the  administration  of  theHC  glands, 
fienenil  painful  clonic,  followed  by  tonic.      Spasm  very  general  and  very  painful,  malolj  in  the  fonn 
■'"'""'•  pnisoning.    Death  usimtly  results  iq  a  couple  of  hours. 

Renerai  permanent  eoalrnclnre.  Paralj-sis  Is  coincident  with  Ihe  contnctore. 

Spnim  only  oocurg      Oeeurs  usually  in  small  muscles  and  in  those  that  have  b«n  overworhed  or  improperly  worked  in  doing  tbe  same  act  many  times.    The  spa»m  is  often  painhit.  and  In  some  eases  pain  may  he    the    only    8>-mptom     (neuralgic  form).     The  spasm   Is  of 
I       performing  graduat  onset  steadily  Rrons  worse,  and  renders  tbe  apcuUoin*d  net  diflicult  or  impo<«ible.     It  occurs  only  when  the  muscles  are  used.     In  some  eases  there  is  tivmor.  in  others  Incoorijinalion  ami  in   rare  eases,  paralptis  or  paresis    (paralytic  forml 

le    necui>tomMl  rather  than  spasm.     Atrophy  of  the  muscles  involveil  is  Gmnmoi.     I'atientH  are  usually  neuratthenlc.     Many  varieties;  writer's,  telegrapher's,  pianist's,  violinist's,  seamstrees',  shoemaker's,  etc..  cramp.    A  shnilar  neuiwis  occneionally  affects  the  Toice 

of  sineers,  public  speakers,  elc. 


Telrtny   (121.  fil.1). 


sirychninp  <(invul5i*.ns  (.11.1,  S'lO). 


Ralhi-r  brief  itpasm 


A  spu*m  lasting  min 
urethral  spasmodii 


Im  or  hours,  due  to  loco!  irrllatioD  inaeunuibeni( 
sirlelurr,  vesical  spasm,  lenesmus.  etc.    S(e  also 


pa  III 


Funclio 


Tonic 
spasm, 

le'Kl.    a 


lirrHixli'Dt      A  spasm  of  varying  intensity  attacking  an  arm,  or  leg.  orbelti.Tiu 

permanent  A  eontmeture  of  a  few  or  many  muscl.si  usunllv  associaltd  with  i 
efforts  are  miidi-  lo  o\errome  It.  No  muaele  atrophy.  Attlm»s  i 
(1174)   or  may  ennsisl  in  jumping  or  skipping   (sjiltotorr  gpumi 


I  (rrfl.0). 
wkwanlnesB  and  often  preve 


Many  \ 


idles.     Hlepharospiism.  loriicollis.  spasmodic  croup,  laryngismus  stridulu<i.  hMncbial  a<thmn.  whooping  i 


uch. 


lopbageal  spasm.      Reflex  spasm   (.Vi'v  '1.17.  llfMl. 


Mental  irritnhilily,  headache,  mn^Tilsions,  astereognosis  and  lomilin',;.  '■iiher  bepnralety  or  two  or  i 


?  combined,  often 


neHthrsiii  of  the  pari.     I'aiially  there  Is  n  combiuatinn  of  apnsm  of  Heior^  and  extensors,  such  as  is  not  seen  in  organic  dl«"ase 
my  lie  -ured  by  ovarian  pn'ssure  or  by  rnrndlaalion.     Oth.-'r  h.vslfrieal  symptoms  (4Ifi).     Ilyslericn!  spasms  are  not  always 


.K    functional    spasm    which    becomeo   greater   Ihe    more 
the  form  of  contr.iotiire.     They  may  consist  iu  trembling 


'Ul    I 


tiaoisl,  eoTrtraelure. 
The  mun'lr«  are 
nnHloiaieally  short- 
ened In  later 
siagen. 


Tendon  reflexes  are  inrreasi'd  when  ttrtpasm  does  not  prevent  Ihi-ir  orsn)rn»nee. 
lasts  for  venrs.     Usually  there  nrefleijn,   „f  yjbow,  wrUl  and  fipTi-rs.  nnd  rstrn 

■Inidon  reflexes  an-  inc^•a«■<l  when  the  ,pii.,|„  does  not  prevent  ilieir  oivurrence. 
an  nltnck  of  paraplegia.     It  Is  of  nry  had  proisuosls. 

Ab.enee  of  reflexes.     Much  muscular  ilKipiiy.     Is  limited  lo  the  distribution  of  ot 
of  tendon  and  fasdn  rather  than  of  ntucte. 


wilb 


The  sjiasm  is  limited  to  the  arm  and  leg  of  the  same  side  and  follows  au  attack  of  apoplexy,  by  a  fe 
a  sclerosis  of  Ihe  pyramidal  tract  and  indicates  a  hopelcM  procnnsis  as  to  recovery  from  the  hemiplegia. 


sfular  atnjphy.     The  spasm,  which  is  often  u'lt 
Follows  disease  of  nueleo-poriphernl  motor  net 


weeks  anil 
ind  folliws 


iiple;:ic  form,  consists  in  flexion  of  both  knf 
Diipuytren's  contracture  si'ems  lo  be  due  to  ooolraction 


.lacksonian  Epilepsy.     (>>rtii'al  irrilation  spasm 
(lKt2). 

Hyslericat  contracture  (107*1). 


Posthemiplegic  e<.n Irs. ■lure   i:m.  :<M.  :.77.  IJHI. 
I'n^t  parapb'Kic  ronlrncture   (r.20,  54n'r.2  SOI). 
Poslneiiritic     contracture.      Ilupujlren's    contM 


e; 


CHART  XIc 
Choreiform  and  Athetoid  Spasm 

Comprising  Numbers  573  and  574  on  left  side  of  Chart 
and  622  to  632  im  right  margin 


149 


DIAGNOSTIC   ANALYS] 


DIAGX03TIC    SYMPTOMS    AND    TESTS 


573 

CHOREIFORM 
SPASM 
(113,126.272) 


G 

E 
N 
E 
R 
A 
L 


TRUE 

CHOREIFORM 

MOVEMENTS 


PSEUDO- 
l  CHOREA 


^Widespread  spas- 
modic contractions 
of  muscles  of  body 
generally. 


Limited  to  one 
group  of  muscles. 

'Sudden,  liglitning- 
like  contractions  of 
groups  of  muscles. 

A  coarse  tremor 
rather  than  cliorei- 
form   movements. 


CHOREIFORM  AND   A 

ABSTRACT   OP  : 

Irregular,  quiclj,  involuntary,  spontaneous  contractions, 
then  of  another  group  of  muscles  throughout  the  body  o 
half  of  the  body  (hemichorea).  Patient  is  restless  and 
is  explosive.  Sounds  are  often  made  involuntarily.  The 
somewhat  the  character  of  purposeful  movement.s.  bui 
closely  extreme  restlessness:  grimaces,  thrusting  out  of- 
of  hands  and  feet,  etc.  Some  muscular  weakness  (chq 
510)  is  present:  and  almost  always  marked  hypotonia 
2.52,  472).  Voluntary  movements  are  interfered  with' 
ordinate  by  the  occurrence  during  them  of  these  Invol 
tions  (ataxia).  The  part  cannot  be  held  still.  Thes 
ments  may  be  slight,  or  so  strong  as  to  prevent  walki' 
speaking.  They  cease  during  sleep,  but  to  some  exten 
They  are  worse  under  observation  and  excitement.  R 
mal  but  the  knee-jerk  may  be  protracted  and  the  foot 
slowly.  Paresthesiae  and  anesthesia  rarely  present.  Th 
deuce  that  chorea  may  be  due  to  disease  of  certain  cereb 
destructive  lesions  of  the  caudate  nucleus  and  of  the 
lenticular  nucleus  produce  the  symptoms  of  chorea. 


Involuntary,  often  unconscious,  or  unnoticed,  execution  ol 
coughing,  hemming,  winking,  etc.     Each  person  nas  hi 

The  spasms  are  instantaneous ;  the  platysma,  stemo-cle 
especially  in  Northern  Italy.  In  the  later  stages,  epih 
ably  not  at  all  related  to  chorea  minor  but  is  more  alii 


Usually   limited    to 
one  extremity. 


Rhythmical  trembling  of  an  extrem 
tunes  more  like  electric  shocks. 
times  called  chorea  magna  or  ma. 


574 

ATHETOID 
SPASM 
(271.  503) 


L 
O 
C 
A 
h 


A  slow  contraction  of  one  set  after  another  of  small  muscles  of  the  hand  ;  rarely  of  the  foot  (mobile  ; 
and  wrists  frequently  also  involvwl  and  are  usually  held  contracuired  in  extreme  flexion.  Squirmin; 
tion  of  fingers,  extension  and  hyperextension  predominating.  The  atheioid  spasm  is  increased  by 
ments  of  the  same  or  of  the  other  hand.  The  face  and  neck  muscles  may  not  infrequently  be  affec 
athetosis.  The  extremity  or  extremities  involved  are  always  weak  bi't  never  paralysed.  The  spasm 
eral  or  bilateral.  Usually  in  hands,  more  rarely  in  feet.  These  movements,  though  slow,  are  powerf 
cause  subluxation  of  joints.     Decided   muscular  rigidity  is  usually  present. 


DF   SYMPTOMS 


ETOED   SPASM 


JPTOMS 

of  one  and 
nited  to  one- 
ety.  Speech 
ements  have 
semble  more 
rue.  twisting 
paralysis — 
atonia  (39, 
made  inco- 
ary  contrac- 
loreie  move- 
3r  eating  or 
:event  sleep, 
ces  are  nor- 
k  back  only 
is  some  evi- 
r  traots.  and 
imen  of  the 


r  Common  in  children,  rare  in  adults.  Slight  mental  disturbances  often 
present.     Usually  acute,   rarely  chronic,   frequently   recurrent.      Often 

I  associated  with  rheumatism  and  endocarditis,  rarely  with  pregnancy 
(chorea  gravidarum).  The  prognosis  is  good,  but  in  pregnancy  is  ser- 
ious and   the  uterus  should  be  emptied. 

In  some  cases  of  chorea,  the  mental  symptoms  usually  present  in  some 
degree,  become  extreme  and  dominate  the  clinical  picture.  In  these 
cases  the  patients  may  exhibit  hallucinations  and  a  maniacal  delirium, 
consciousness  may  be  clouded  and  the  intellect  may  progressively  de- 
I  generate  into  dementia.  This  form  of  chorea  runs  its  course  with 
fever,  is  most  common  in  adult  pregnant  women  and  frequently  ter- 
minates fatally. 

Occurs  only  in  adults.  There  is  much  and  progressive  mental  impairment. 
Movements  coarser  and  more  violent.     Heredity.     Chronic. 

Occurs  only  in  old  persons  with  atheromatous  arteries  and  brain  symp- 
toms.    It  is  usually  progressive  and  the  mortality  is  rather  high. 

Occurs  in  hemiplegia,    (after  apoplexy,  etc.)    and  is  confined   to   the  in- 
completely paralyzed  extremities,  especially  the  hand  and  arm.     It  is 
most    frequent    in    the    hemiplegias    of   childhood.     Sometimes    a    pre- 
v     hemiplegic  form  is  met  with. 

e  same  act  at  short  intervals.  Little  "tricks"  which  characterize  many  persons  such  as 
pvn  individual  trick  or  habit  and  rarely  varies  from  it.     Usually  occurs  in  neurasthenics. 

mastoid  and  hypoglossus  muscles  are  especially  affected.  It  is  a  rare  disease,  occurring 
form  convulsions  and  paralyses  with  atrophy  occur.  Often  fatal.  This  disease  is  prob- 
jo  myoclonus  (600-1). 

varying  in  intensity.  At  times  so  coarse  and  irregular  as  to  resemble  chorea,  at  other 
er  symptoms  of  hysteria  present  (415).  The  extensive  convulsive  movements  some- 
(27.3)     are  purely  hysterical  and  are  not  choreic  in  their  nature. 

The  athetoid  spasm  is  present  from  birth.  It  is  very  rarely  unilateral, 
more  frequently  bilateral.  There  is  much  mental  impairment,  even 
idiocy. 

in  bilateral  -j  Present  from  birth  or  infancy.  Some  mental  impairment.  Unilateral  or 
7  be  unilat-  bilateral.    Associated  with  a  mild  hemiplegia  or  diplegia.     Rare. 

Occurs  in  adult  life  after  an  attack  of  apoplexy.  Usually  unilateral. 
Rare. 


im).  Ankles 
wistlng  mo- 
itary  move- 


md  at  times 


DIAGNOSIS 

Sydenham's,   or   Infectious,   Ohorea.     622 
Chorea  Minor   (272). 


Chorea  Insaniens. 


623 


Huntington's,  or  Hereditary,  Chorea  624 
(103). 

Senile,  or  Degenerative,  Chorea.  625 

Post-hemiplegie  Chorea,   (501)  626 


Habit     Ohorea     or     Habit     Spasm     627 
(274), 

Electric   Ohorea.    Dubini's   Disease    628 
(.597). 


Rhythmical,    or  Hysterical,    Ohorea     629 

(273). 


Congenital  Athetosis,    (501). 


630 


Athetosis     after     cerebral    palsy   of    631 
childhood,   (501). 


.Athetosis  after  apoplexy,   (503). 


632 


CHART  XII 

Perversion  of  Motion  and 
Local  Palsies  and  Spasms 


DIAGNOSTIC  ANALYSIS  OF  SYMPTOMS 
Symptoms  Analysed  Character 


635 
PERVERSIONS 

OF  MOTION 

(243) 


("638 
ATAXIA  (248) 

639 

TREMOR  (250) 

640 

NYSTAGMUS  (292) 

641 

FIBRILLARY  CONTRACTION 
OR  FIBRILLATION  (293) 


The  diseases  in  which  ataxia  occurs  are 
set  forth  in  Chart  Xlla. 


The    diseases    in    which  tremor,  nystag- 
i-     mus,  or  fibrillation  occurs  are  set  forth 
in  Chart  Xllb. 


LOCAL  PALSIES  AND  LOCAL  SPASMS 


636 

LOCAL  PALSIES 

637 

LOCAL  SPASMS 


See  Chart  XIIc. 


See  Chart  Xlld. 


149 


CHART  Xlla 


Ataxia 


Comprising  Numbers  638  and  642  to  644  on  left  side  of  Chart 
and  647  to  664  on  right  margin 


151 


L/IAGNOSTIC    SYMPTOMS    AND    TESTS 


(M2 

lia      ro  a  J  D  I  7 
n    vrnDitiDg    or 

nfllkiDi;.      Stiiggn- 

JDR  (^ail. 

Sialic  alalia. 

(VrobPllnr  niniia. 

(2S1>. 


loabilitf    to    tlaad 
inlk.     Mnre  or 

complete. 


IVH 

tin  of  all  II 

nyonmic  alaxi 
(2S0). 


nnllnt^rnl, 
(UcmiBtaxia.) 


I'ritla(-nl. 

Illnmial/iiln.) 


Irrejoilar 
distrlbiitlnD. 


I  Oemirj  at  any  age. 
usually  Id  adults. 
'  I'liially  wnwry 


BIAGNOSTIC   ANALYSIS   OP   SYMPTOMS 

ABSTRACT   OK   SYMPTOMS 

Patient  exhibits  the  itasgering,  irn-inilar  gall  of  a  drunlteii  man.  I.illle  ntaxia  of  niov*mpnt«  of  hands,  or  of  leea  when  Ijlng  down.  Vertigo,  vomitini;  and  heodafiit;  nre  often  present, 
nystai^us  may  lip  iitesent  (tumorel.  Knee-jerlis  may  be  presni  or  nl>*?nt  (u<iiinll,v  pncpnu.  Cerebpllar  file  (fiOO-lO)  may  owiir.  S^mpionu  may  be  bllntera!  or  unilateral  (same 
Hj'jiuruata  is  pieseni.  uUo  a  dindocoldnesiii  (3C)  due  In  a  long  outintinnri?  of  mii"ailnr  contraction.  Patient  can  lie  on  ba<^k  ivilb  lc;s  Dex«l  at  hip4  und  knees  miich  longer  than  a  d 
v-vy  mnrti  longer  Ihnn  pali'-nls  with  ilynnmic  ntnsin.  When  the  cerehellar  irncls  in  the  brain  jitem  are  involved  by  the  lf<>ion.  cnnilguous  iracta  may  niso  b"  io'ralveil  in  n*ich  cane  thrrr  \ 
«en«nry  symptning  in  the  arms  iind  legs  and  diHlurbancra  in  the  domain  of  thi-  irsninl  nerves,  miially  unilateral,  nnd  laryioE  in  character  according  lo  the  gent  of  the  lesion. 


Choked  disc  or 
side  ns  It^ion). 
>nnn1  pemnn  and 
rill  hr  motor  and 


No   loss   of   miisrle 
»i-n«e.      No     motor   , 
pHro1y«i«,  except  is 
late  iitat.'V  of  050-1, 


Sinegerinc    enti,  constantly    or    psroxj«-     j  Diplopia 
mally.     Hendsrhe.  verlico  and  vomiting    J 
at  limes.     No  cbokrf  disc.     Knee-jerks     1  hejifne^h 


other  diBorders  of  hiBhl.     Vertigo  ceases  when  eyes  are  eloied. 
il  rini;ina  in  nm-  ear.     Pniv>ty*nml  iiltscks  of  mtenBC  vertigo  and  defect  in  l>"nf 


Occurs  in  youth. 
I  No  lenury  aymp- 
1  loma. 


Many  seiuory 
symptoms. 

Oft'n  nnalee»ia 
and  thermic 
aneatbena. 


liriiTi  ID  family  groups  and  ^hows  well  marked  her^'dnv 
though  leit  pronounced.  A  general,  conree.  irregii'or  ii 
Blstimus  is  common  and  speech  often  defective.     Synpicn 


nr,  limulitling  jerky  choreiform  mwementB.  Ny- 
!iri'ient  n  mixture  of  weohness  and  ataxia. 


rOcciir*  after 

1  Occurs  befor 
'■     UKDnlly  pn 


puberty.     Knee-jerks  present.     Oculnr  parn'j -i' 


before  pDberty.     Kneejerkig  absent,  except   i 
iHy  present,    Opiic  slroi>hy  rare.    Club-foot  cc 


.  of  ptipil   reftes  nnd   opti 
p   and    m    exceptional    ca- 


st ropby 
>.       Babinehi 


ICvidently  organ tc. 


l^e<>  can  be  mov<^l  nisily  in  nil  directions  without  ataxia  wh 
Simulatea  an  nprnxia  I2:n)  rather  th»n  nn  nlnxia.    Often 

May  or  niny  not  be  motor  parnlysi 
lia  while  walking. 


'ul  il  lying  down,  but  collapite  when  tihe  tries  to  walk,  or  after  nalk.ng  a  few  stept.  nppnrrnlly  from  lack  of  confidence 
emiilicnal  cause  and  hjDlerical  vrap'<>''>3  (415)  are  present.  Both  leA  are  inrolwd.    Never  hurts  herielf  Eerlously. 


of  same  side  with  iifialgesta  and  iher 


Lou  of  muscle 
Nense  and  §pniiory 
symptom  R  umnlly 
prominent.  Knee- 
jerk     imually     1d- 


When  of  acule  course  the  condition  uiu- 
ally  folloivs  an  apoplectic  attack.  Often 
arlerial  dispane  is  preaeni,  When  of 
chmnic  cour*e  chok'd  disc  may  be 
present. 


■Mnrked  uneslhcain  wilhoiit  analgetiin.     No  motor  [laralysiH.     No  other  symptoms. 

.Apoplectiform  atinck  followed  by  hemiplegia   {Keiinory  ofti-mr  than  motor).     Other 
where  the  motor  paraly^iis  wa*  slight. 


itesthesia  of  conlrulatcrnl  side.     One  leg  only  involved. 

Very  rare.     May  be  the  earliest  stage  of  a  -ipjnal  tiini 
poBt-hemiple^ic  motor  disturbance?  are  often  iiresi-nt. 


reflex 
will  power. 
No  ataxia  when  moving  leg  while  lying 


ir.     Unilalpral  later  becoming  bilateral. 
The  ataxin  ofcnrs  iu  convulrseence  in  i 


Knei'-jerkn   normal.      No  ankte'Clonu*.      History  of  alt'i>liuli>>n 


There  are  often  niHxiii  nnd  K 
nrlhriu  and  paralysis  of  v; 

i^igns  of  cortical  irrilalion    (' 

il  and  foolish  speech. 


Hli 


Ala 


Rincgerated  knee- 
iprh«,  nnUeclontis 
nnd  nnblnnki. 


Knee  jerki  nnd  aii- 
kl^.-lonu«  alwenl. 
No  Rnhinski.  Oftm 
loK»  nf  munele  nenie 
and  retardnlion  of 
roniliiclion  of  pnin. 


ireal  vari"ly  of  local  «j-mploms.  I'sunllv  Imih  motor  and  rnumory  Nyinptoms.  Irregular,  jerk.v,  alax 
inientton  tremor,  scanning  upeeeli.  nj^lagmu*.  espeptnlly  on  motion  of  eyeball,  nnd  ittropliy  of  op 
Rarely  llie  diseuee  runs  an  acute  coiira-  and  has  bem  called  "acule  ataxia,"  of  which  therp  are 
18  tiie  presence  of  symptoms  only  explicablr  on  the  n^umption  of  Ihe  exiateuce  of  levernl.  se[mr 


if  iiMiscle  setiRe  on  one  side  of  body  nnd  analgesia  and  Ibcrmii: 
IS  cranial  nerves  arc  UHually  present, 

iilkiuus).     Anestbe«ia,  cupecinlly  loss  of  muscle  sense.  Is  oflet 
;in  and  other  symiilotii's.     Temporary  ti-emor. 
mcnl! 


m^y  be  crossed  parulysi* 
III  me  mental  disturbance. 


if  both  arm«  and  legs,  and  movements  are 
!■  nerve.  In  some  ernes  huHmr  paral.vsis  (434*  is  aneai 
'v?r:il  varieties  (662).  In  its  early  stages  the  diacnoK 
e.  small  lesions. 


I  of  this  discnse  i 


r.ittle 


\  rombinalion  of  symptoms  of  locomotor  ataiin    (tWl)   nnd  spastic  parnple.-in    fH'-in)   in  veryin:;  t'i"l'"i''i 

usually  lost  before  any  nnewtheHia  can  be  deleeleil.     In  later  slnces  arms  may  he  somewhat  involied.    .V  riir.-  disc 
jerks  may  be  ahclished  towards  the  end  of  the  disease,  but  Babinehi  persists.    This  disiase  iniiy  be  caused  by  pi 


r  nn  pnin.     WenknesK,  slilfness,  ninxia,  pare^theii 
ncensionally  some  involvement  of  cranial  nerves 
ions  and  other  severe  anemiias. 


I  Slight  motor  iiaraljsU  i*  present,     Miisflen  lender  and  atrophic.    Pnin*  rardy  ' 

normal.     Cranial  nerves  rnrely  Invulved.     Usually  sensory  sj-mptnnis,     UbiiiiII 

I      never  so  chronic  as  tabes.     No  globniin  or  b-mpbm-yiosiN  in  crrebro-splnal  fliii 

-„„-,,„  I,  .J     ,    .  rHl«tory   of   taking   dnie«,   alcohol,   mor-  The  alaxi 

.npjerks  usually  exnirgerated     hut    no  I      phine.  ver^nnl.  cocaine,  heroin,  etc  nnd  exc 

itnbiDski    or    ankle-clonus.     Evidently  1 

functional    (pseudo-alaxia).  1  Dmorionnl  cause. 


ry  severe  and  partial  re.i 
history  of  nicohniie  nbii" 
Prognosis  is  good. 


of  degenenition  and  retardation  of  cnndueilon    of   pi 
Ii'iitnl  dii^turlinnccs  in  many  cases.  Ocen«ionnlly  the 


■iflei 


leil  with  tremor  and  neurasthenic  symptom?.    Failure 
ted  with  c 


'Til?  ntnxia  may  appear  only  when  eyes  are  closed  nnd  is  usually 
usually  collapse  on  reactiiug  a  place  of  anfety. 


signs  of  mental  impairment.     Patients  nr^  emotional 

tcrir-nl  symptoms  (415)  tin  pre-sent.     Rarely  fall,  but 


T^-eaion  of  ccri'bellum  or  ita  tractsi:  if  acute  in  onset, 
apoplexy:    if    chronic,    tumor,    or    inllammalion. 

inoT-'i.  ci.-.;j,  ftso.  Tft4.  i>iw.  utm.  I2fl5i. 


Ocular  ataxia  or  verticw  (1020). 


.Marl>''s  biTpditary  cerebellar  ataxia 

(iMH),  l'il\. 
rri'-dnich's    Piecise.      Ilrredilary    Ataxia 

(104.  124,  G71).  (187,  705.  7S2). 

Astoula  and  Abasia  (2S7.  7IW). 

l.esion  of  Infernl  column  of  i^iniil  cord,  ir 
dircfl  cerebellar  tract  (017.  l.'|tin-73.  1100 
(f-'ie..  24-7.) 


onn 
em 

(iri2 

IK3 


LeHnn  of  i.'".lerior  niluuin  of  cord    (780,  I3»]0;t-4. 

140H),     (KigH.  24-71. 
Posl-liemiplcaie  ataxia    (h-siun  in  or  near  posterior 

part  of  opilc  thalamus— 1208.  13981.     (Fig.  17). 

.'Softening,  heiuorrhasc  nr  tumor  In  brain  stem 
C^M.  et.  si.i„  S.T.i.  T.-ilO-T).     (I''!iP>.  10-22). 

•Softenina  or  tumor  of  conlmlateral  iiurietal  cortex 
(I30S-75.  1:«12).     (Fig,  IG). 

Alcibollo  intoxication  (lltS.  101-2.  {iST.,  003.  1173, 


1  vpaslic  and  al.ixic.  Very  characlcrlHiie  are 
I-  often  einotinmil  and  exhihil  mental  weaknes. 
exeeed!u;;ly  difficult.    The  most  essi'utlnl  point 

le  and  anesthesia  of  legs.     Vibration  sense    (50.  353)    is 
Orgnnie  reflexes  slightly,  or  not  nt  all,  disordered.  Knee- 


tarely  any  perninncnl  motor  paralysis:  hut  hypnlonln  (2.">2).  allowing  hypcfe.x tension  nnd  extreme  mobility  of  joints,  is  common,  and  tempomry  paralysee  In  thr  domain  of  the  crania]  nerves  fcspecinlly  the  muscles  of  eyeball) 
are  not  lux-cnimon  eiirly  symptoms.  MovemenlH  nre  atoxic,  ipiick,  violent,  excess tve  and  constantly  conlrolled  by  eyesight.  The  nffeclefl  pans  ennnoi  lie  held  motionle**  in  onn  position  lone.  In  wnlklnc.  legs  nre  held  well 
ntmri  and  feel  are  (luue  loo  far  outwani  and  too  far  forwani  nnd  are  brought  back  hard  on  heel.  Ataxin  niiich  worse  when  eyes  at*  closed.  Walking  in  thr  dark  or  luickwnrds  is  usunll.v  impossible.  Romberg's  symptom 
(4:tS).  Argyll  Unberlson  phenomenon  (437),  luyosis,  nnd  optic  alniphy  with  concentric  liniilation  of  fii-ld  of  vision  are  common.  Lighlnin?  pains  .»f  great  intensity  in  tnial!  .in-as  followed  by  h.nieralgr*in.  girdle  senitalioiis 
and  paresllnsiae  ar-  prominent  sympl.mis.  (Irgaiiie  n>(lpxes,  espe<'ially  Ihe  vesical,  nre  disordered,  Artliropathies  (1188)  or  perforating  ulcer  or  o'lier  trophic  disonlers  may  h.-  present.  Ani'slbesin  and  nnalgesia  in  patches 
and  in  cuirass,  ulnar  hypere«t1iesia.  Retardation  of  conduction  of  pain.  Visceral  crises  (O^^Tl  are  tinuatly  presenl.  Townnls  the  end  of  the  diaease  motor  pnrnlyiiis  may  appear.  lymphocytosis  and  globulin  In  cerebro-spinal 
(luld.  The  discnsc  is  unmetime*  dividiil  Into  tlir.-i.  WjiRrs-dst),  the  neuralgic;  (2nd),  th"  ataxic;  (3nn,  the  paralytic  slage.  History  or  other  evidences  of  syphilis  or  of  venepenl  disease  is  iwLiolly  present.  Positive 
Wflsirermann  also  usually  prenenl.  There  are  several  forms  of  tnbps.  In  the  cerehrnl  form,  atrophy  of  ihe  oplie  nerve  is  the  prominent  symptom  nnd  the  legs  show  little  atnxln.  In  cervinil  tabes  the  arms  are  mainly 
alfeel-d,  In  the  orrlinnry  fonn  the  legs  ,irc  mainly  afftH'iefl,  In  all  forms  the  knee-jerk,  are  nb-senl.  Babi(i>tki  i<  present  in  rnrc  cnses.  compllcnle.1  hy  lat.-rnl  sclerosis.  In  miny  case«  ef  tabes  the  ataxia  is  slight  and  the 
diniinoslh  musi  n-sl  mainly  on  the  obwnee  of  the  knee-jerk,  the  Arcyll-Roherlson   phenomenon    and    the  ceiebro-»piunl    Ijinphocytosis.    together   with  wbatcMT  other  syiniitom*  may  bo  present. 


JU*'ioitiati-d  Sclirosis.     Myelitis  Diswminala. 
Kncephaloin.i-eIlti«    (Ml.   5S0,    Ot«l,   ttSS.    750-68. 
^m.  1)14,  1054). 

Uaxic  Paruplegia.     rombinnl  Sclerosis 
(:.2tl.  TP9).     (Fign.  24-«). 

.ni-i>ni<  lor  Ataxia.    Tnlic«  Dopsiilis 
(i:tj,   1T:i.    123    T.TH.  7«.  820-71-00.  fll2-7I)-8S, 
ItMM,   1172W1.   1217-31).      (Figs.  24-6). 


Mullipli-  Neuritis.  I'ol.vrn-iinlH.  I'si'iido-labes 
(KV  7SD.  s.2ii.  niOS.  1117.  I.'t27>. 


r»rug  habit    (toxic)    (482.  058.  707-81). 
Ilyslerieal   Alaila    (1070). 


CHART  Xllb 


Tremor,  Nystagmus,  Fibrillation 


Comprising  Numbers  639  to  647  on  left  side  of  Chart 
and  666  to  697  on  right  margin 


153 


DIAGNOSTIC    SYMPTOMS    AND    TESTS 


InUDtloo    TrMDor 
(281). 


tremor;  4  to  S  jit 


or  is  iHiisDy  nssiicinK^  ivllh  sojmniiiB  spre^li.  n.vMafmu^.  atropliy  "f  opt 
nllv  a  Brmit  »*nrii'ty  of  motnr  in'l  sensory  symptoms  iliie  to  mnni 
inlly  wirh  tlieir  loss,  over  a  vory  vnrinble  area.  The  sensory  •jmpl< 
n  symprrtm. 


DIAGNOSTIC   ANALYSIS   OF   SYMPTOMS 

ABSTRACT  OP  SYMPTOMS 
nene  nnd  ataxia.   Reflexes  are  ii«unlty  exnggersted  and  ankif-i-lnniis  nnd  Bnl>in«ki  are  present.     In  some  caees  the  deep  rellcii-s  are  early  abolished   and    Ih^  orsanic  reflexM  dUordered. 
ns.  alihniish  all  the^e  mny  hp  nbannl.    The  mntor  symptfim^  nirntnente  ;ia  fntigtie.  slowly  becoming  paresis,  rarely  paralysis,  nrd  are  u^uiilly  as*oeini*«l  wirh  pjnggerated    refleies.  ocea- 
usually  in  tlie  form  of  paresthesiae,  more  rnrelj  pain  followed  by  Irregular  patches  of  anesthesia.     Epileptiform  or  apiplei'iili>rm   atincks   tollowod   by   transitory  paralyale  are  commoo. 


Oi^cur?  in  family  groups,  but  Is  neithri 
hereditary  nor  eoneenital. 


Occurs  in  family  groups  and  shows  tc^II 
mnrlcKd  heredity.  Slarserin;:  gaii. 
Ataxin.  NyBiagmns  is 
speech  oftno  defective. 


OcTur^  ID  yoiirm  ppnon?. 
athptosh.  nnd  prngresn 
auiopiiy   there  is  found 


Tri^noi 


I  nuncinlrd  with  general  wenknt 


fFine,  rapid  tremor; 
S  to  12  per  aecood. 


Pawiive        Trpnior.  I 

]  iDcreAMM)    on    rol-  J 

imtiiry  motion  and  | 

excitement  (200).  i 


^lophtbnltnii:. 
mnllj-  wh*n 


eo'iitp.  tiirhyrardla,  vasi-ulnr  Ihrobtiing,  fluKhing.  »npniin'i. 
ifltient  look*  dOTt'award   (nraete's  srmploml.     The  ^.-^ijiro  i 


nilaleral.  rhythmionl  tremor,  whlcli  increjses  on  voluntary  movements.  There  are,  also,  djsnrlhria.  dyspliasia.  mmcular  w-ahm'^v  «pn»llelty  and  controoturee.  Mpecinlly  facial  Kriraace*  and 
,c  pmBointion.  Thr  refleies,  superfleini  and  deep,  are  normal.  The  patient  is  emotional,  present*  various  mental  eymploms.  a  pro?rt-i«ive  dementia  ind  the  disease  has  a  fatal  termination.  .\l  the 
1  bilateral  symuietrioal  degenerRtion  of  the  putnmcn  and  trlobus  pntlidus  of  the  nucleus  lenticularis.    Another  lesion,  constantly  found,  is  hepntic  cirrhosis,  which  produi^s  no  symptoms  during  life. 


nd  exceptional  case*.     Babinski  i»  present.     Optic  atrophy  rare.     Clnb-foot  common.     Rfliely  sensory  sj-mptom:  an-  prcent. 

evidence  of  any  organic  disease  of  the  nen-ous  syntem.     Bxhausl4on  or  holding  a  limb  in  n  ntraineil  position  Cnr  a  long  lime  cauic*  tremor. 

'^fcilement.  polyuria  and  at  limes  albuminuria,  insomnia  and  vorli;:o  are  common  symptoms.    Tbc  upper  lid  does  not  fall  nor- 


Oecur 

after  puberty.    Ko'''  jerks  are  present.     Ocula 

r  paralysis,  los«  of  pi 

Orrur 

before  puberty.    Kii'e  jerks  arc  ah=ent  except 

in  early  atage  or  in  ra 

s  or  K 

onvalpscnce  from  nn  acute  disease.     Anemia 

•>  usually  present,  but 

rliarriioea,  much  nrrvniisne's,  tremor  rspecinlty  marked 
.  of  tb-  porcncbymotouv  variety  and  noed  not  be  large. 


Ili*tory  of  ndiicllon  to  alcohol  or  liruc*.     Mental  symptoms  are  common. 
arratly  at  different  times, 

Preiience  of  hysterical  symptoms  (4151.    Tremor  is  w-jrwe  when  ailpotion  i 

Tremor  i*  m.irk«l  tn  fncp.  lips  and  touEue  :    n 

r^umhnr  puncture  shows  a  lymphocytosis  and  globuli 


and  judgment  impair 
1  it.     Irn>eulnr  tremoi 


I  and  Hppprh  blurred 
Evidenc"'  of  great  rxh 


Pati. 


i  and  emolinnal.     Pupils 


ictcd   i 


opium  <: 


Qninqunnd'*  'rign   (4."iSl    in  alcoholic  cnwv     Symptor 


•,     Proures'tivi'  mcnbil  impairment.     Reslless  and  chlldiiih. 
W,i5*ern>ann  reiction   usually  positive.     Arcyll-Roberlsr 


ijstem.     Often  history  of  slight  injury  assoeialpd  i 
and  letters.     Apopli-cliforr 


Snecrti  is  slurreti  by  elision  of  nyllnbli 
phenomenon  is  present. 


ilb   fright,  or.  more  commonly,  of  tri),'ht  alone. 
and  epilpplifonn  attacks  may  oivitr.     History  of  nyphilis 


Slow  tremor  of  hand  and  fool  of  same  side. 


iated  with  oculo-moir>r  pnrn 


nt  tlic  oppcsite  side.    Other  sj-mptoi 


«of  a 


G4(ta 

Passive       Tremor. 
Diminiibed  on  vol- 
untary motion 
(290). 

Eithi^T  Inlentinn  or 


Always  a  symptom 
of  organic  disease. 
Very  rarely,  an 
hyjiterlcBl  clonic 
■pasm  may  aimu 
late  true  nyitag- 
mue  (pseudo-nys- 
tagmus). This  ia 
often  vertical  and 
is  more  rapid  and 
more  violent  than 
ny«ta([mu«  nod  is 
na5ociate<l  with 
other  hysterical 
■jTOptoms  (4ir.). 


ISIow  tremor:  3  to 
fi  per  second. 

r  Slow,  fine  tremor; 
,3  to  6  per  second. 


Treaior.  nhicti  is  fliwciated  with  muscular  rieidity  and  mash  like  f.ic  nniisi<it«  of  "nill  rollinc"  movements  nf  hnacrx  and  genernl  tr^mn 
and  l^nillv  involves  the  other  side.  The  tremor  is  moct  marked  in  tbr  finuers  and  hands;  tb"  hpad  and  body  csi-ipp,  except  in  very  ran' 
Vinci's,  niaractiriatic  attitude  thead  and  body  bent  forward,  elhiiw.  Ileircl.  hnrcfi  sliehtlv  flevcH  i  and  festinatinc  call  or  prnpnl?!  in  . 
lie  lll^^  n  similar  tendency  to  run  backwards  Iretmpulsion).    Tin- iiUitudc.  (."nit  and  mn»k-like  face  are  all  due  to  muscular  riciilitv  nl 

sine  niriiiiiionel.     The  fiisensc  often  cnmrnencps  with  a  stiffnesi  ao'l  ■.Foivn""  of  niovi-ment  of  oup  arm  or  hand,  wmulatine  n  mild  r 

There  aip  no  senwry  sj-mploms  PKCPpt  the  aenaatlon  of  rlzitlity  and  :i  fcclinir  uf  heit,  n-hich  arc  frequent  and  dislrcfwinp  symptoni'.. 
argica    fHHTt.     DcBtnictlve  lesions  of  the  pallidal  system    (globus  pnlllrfuo  of  the  ienllriilnr  nucleu"!  produces  the  symptoms  of  piral 


brain  lesion.     May  be  aspsoclnipd  nilh  hemipli^^ia, 
■hich  commcnceH  In  on?  cxtiemily,  later 


r  motor. 


r  treases  durini:  sleep  and  is  incrcaseil  i 


citcmetil. 


(lil.v,  later  extends  to  ihc  other  extremity  of  Phe  »nm-  side  (rarely  to  that  of  the  oppoHle  hide), 
i-ommencei  after  forty  years  nf  aire  and  proarenses  nlonjy.  The  tremor  usually  hrcome*  coarser  In  tlie  later 
11  forward  which  compels  patient  In  walk  faster  and  finnlly  to  nin  until  he  fall-  focnards  or  against  an  obstacle. 
it»rist'c  of  tbc  iti-sPTi^p  than  ic  the  Iwmor,  and  in  rare  cases  occur')  alone  v>itlioul  any  tremor  fpntiil.'miH  asitans 
ing  Inter.     Voluntory  movoments  arc  slew,  much  rcilrfctcd  and  feehte,  but  arc  never  comnlplely  paralyned. 


t  entirely  hplples^.     Marked  symptoms  of  parn 


agitni 


:^'iir.   not   infrciiiicrilly   in   Encephalitis    l.cth- 


r  begins  tii  late  rally.     Head  is  early  affected,     Nodding  movem 


Slow,  coarrie 

1  tremor. 

I'ossive  Tremor. 


f  Rotatory  or 
J      volved.    1 

I A  series  of  . 


noddin:  tremor  of  head  occurrine  suddpnly  in  rickety  babies 
The  tremor  ceases  when  the  child's  eyes  are  closed. 


I  Iht 


risidity.     Rf 


eral  weakness,     .\thpi 
'  and  passing  off  in  ll 


mntous  artorles 
summer  time. 


Usually  accompanied  by  n.vstagmi 


jerky  treraoni  limited  to  the  back,  or  Involving  all  ninscle^.  enused  by  cold  (physiological)  or  Infection   (pathological)   onrl  resulting  in  an  inr 
Not  ■eociated  with  other  symptoms.     Hereditary  basis    (a1cohoIi<ra  in  ancestor*,  etc.).     May  be  locil  or  general.    Usually  in  advanced  age- 

Ti  [Defective  vision  from  whatever  oanse.  conginltal  or  squired,  in  early  childhood.     Often  associated  with  blcpharo<ipnsm  and  oscillation  of  bead. 
Due  to  lack  of  pigment  in  iris,  choroid,  etc,    tTgwally  nieociated  with  pbotophohln. 

Workers  in  mines.    Due  to  working  in  poor  llah*  and  looking  sideways  constantly  while  at  work.    Richt  grows  steadily  worst  and  siisn.i  of  nervous  exhaustion    ( 

in  Hie  opposite  di 


'hich  crows  worse  when  the  child's  head  is  held  s 
the  body's  temperatnire  and  may  be  followed  b>  high  (evf 


Impnirment  of 
sight 


Vertigo  is  a  promt- 
I  Dent  symptom, 

I  Coarse,  jerky  tre- 
mor is  a  prominent 
I  symptom.  .\taxla 
J  is  also  present. 


lent' 


lal  aitflcks  of  rertico  a«sociated  with  deafness  and  tinnitus  aurium  and  due  to  disease  of  inner  ear.     Ny 
or  cali-aniKcd.  or  ear  syrinced.  or  labyrinth  In  any  way  irritated.     The  caloric  reaction  (70)  is  absent. 


Tihlynpia.  nyitagmus.  tics  a 
ection   from  the  lahiTinth  i 


volved  oceun 


iiilTy   when  head   is   rotated   vlo- 


Vertigo,  cerebellar  alsiin  and  other  sj-mpioms  of  diniease  of  the  cerehelluin.     The  nystagmus  is  ustially  towards  the  side  of  the  lesion. 

[Occnra  In  early  .vouth.    Strong  hpredltj'.     Knee-jerks  nbsent.  except  in  early  stage,     Rahloski  Is  present.     Optic  atrophy  rare     Muscular  vreaknere  and  contractures  are  not  uncommon 

Occurs  at  any  age.    No  heredity     Intention  tremor.     Eiagjiemted  knee-jerk,  Babinski.  optic  atrophy  and  scnnnine  speech  are  common  symptoms.     Vertiso  Is  ii5unlly  present  (0321,     r,rfical  paralyses  common, 
Orynirs  In  mi-ninsiris  and  in  local  lesions  (tumors  eapeeially).    Nystagmus  U  commonly  present  in  bulbar  lenions,  especially  in  those  involving  the  ccrwbellflr  peduncles  and  tracts  and  the  posterior  longitudinal  bundle. 

to  be  confounded  with  the  deep  bowing  fSataam  crampl  which  occurs  in  some  idiots  and  enilepties,  with  or  without 


Th*  nyataemus  is  most  marked  when  the  child's  head  Is  held  still  and  the  tremor  prei'ented  (flTD). 
nystagmus,     RoUiD!  of  the  head  may  occur  In  otitis  media  and  in  rickety  chtldr-n. 


or   more  of   the   recti 


VIHRII.T.AIIV  c-n 
TR,\(TTION  OR 
PIHUn.I>,\TION 


Kvidence  of  orcnnic 
dUease.     DcEenera-       atr. 

I  li'm    nf    peripheral      ruli 

1  motor   opuront. 


Marked  miiscul 
ly  with  mi 
weakness, 


I.  Congenital, 
Nystagmus  ( 


Marked  sensory 
sjTnptoms, 


T.a 


eral  oscillating  nystagmus  associated  with  jerking  movements  of  the  limbs  or  trunk.  osBravatiHl  by  cold  and  by  percussion.     Associated  with  other 
■alescencc  frcm  ocul.ir  palsies  or  when  weakened  muscles  are  stronaly  exerted. 


li'tocw. 


Bvidence    o!    func-      No  muscular    atro- 
tional,  not  organic,      phy  or  weflkness. 


.Analgesia  and  thermic  anestheela  witti  m 

.Mii«<ular  atrophy  anil  flhrillnry  enntractii 

Muscular  atrophy  and  fibrillary  ontrarii 

Muscular  atrophy  and  fibrillary  contraction  of  thp  peronei 

Occurs  usually  tn  orhtcutarls  palpebrarum  but  may  occur  1 


lutiraiion,     .Slight    tactile  impressions 


ly  slight  anesthesia,  or  none  at  all.     Tronhic  disturbance 

in  of  tongue  and  lips,  dysnrtlirifl.  dysphagia  and  spastic  paraplcfria. 

on  of  Kinall  muscles  of  hands  and  of  shouldor  girdle  oomhmed  with  spastic  paraplegia. 

Bcles,     Rarely  there  nee  pain.  muscl«  twitrhlng  and  niicsthesla. 

ny  moselB      tt  cnnMsts  in  a  quivering  of  the  muscle  fibers  and  occur*  In  tiitira sthenic  an  J  exhausted  persons. 


Multiple  Sclerosis. 
I. -ill.  .-.SO.  IKO- 


DIAGNOSIS 
rii"eminiited  Sclerniif. 
IS.  "iG-OS.  803,  OH.  lOM). 


.Symptom-  retembling  sfty  clo»el>  those  of  multiple  sclerosis,  but  (be  ir^oior  presents  a  tnily  oscillatory  character  and  there  is  no  real  ataxia.  Emotional  and  maniacal  attacka  may  occur  and,  less  c-'mnionl.v.  mental  confiisiun  and  hallucinations.  Many  of  the  cases 
r'scmhl'  closely,  if  they  are  not  idenliiml  with,  dystrophia  leotieular**.  The  lesions  iu  lhi,s  disease  vary  greatly  in  the  different  caies  which  have  been  examined  after  death.  In  some  cases  there  is  utronhy  of  the  cprcbral  convolutions,  in  others  degeneration  of  the 
Isniicnlttr  nucleus  and  very  commonly  htions  of  the  glia  cells. 


'roiire^.iie  I,pnticiilar  Degeaerntlon.  Wilson's 
Di»i'rt»e,  Dystonia  (.entlculnris  is  closely  allied 
to  the^e  syndrom". 


Friedreich"*  Hereditary  Atasin. 

ir,.*,I.  BS7.  7nr«.  7«il. 
.\sthenio  Tnminr  or  weaknewi,  (702). 


I'Uophthalmic  (ioitrc.     Rnsedow's 
(JmvW  Disease.  (HlB). 


llj^terinil  or  N' 

matic  Npup.ist 

Paralytic  liemi' 


nthenii- 


L'otlnc.   mercury, 
and  also  Trau- 


1071-71 

■nerat   I'arcsis.     riiresis.         ii7.* 

(i:iri-77-vt(,  .ion-12-a   r.Tft.  7««,  s!i7,  lOfii'.  iioti, 

12H!,   lUrtiJi. 

■si  >n  of  th"  Criis  (Vrchri  or  Pons  Involving  the     Srf 

Rubro-'piii.il  trwci.  (ISl.  1203.  1341),  (Figs.  18-30). 


'anily*i»  .\:itiinv     Parkin. 
(ilKI,  7iM».  WMl 


.  IHse 


077 


Senile  Tremor.  ' 

Spasmus  Nuttms.     Nictilatio  Spn»tica,    (liWI.  t 

Chills.    Risoi^    Shlverine,  • 

Essential  Tremor.  * 

Atnblyopla,   (3.-i9).  ' 

Albinism.  ' 

Miner's  Nystagmus.  ' 

Meuitn-'*  Disease,     Aural  vertlpi.     Ijihyrlntliine         I 
Vertigo.  (040,  ItlS.  1019). 

rerebellar  Di«en*e.  (fl07-?.  fWO.  7&4,  1016.  ISn,*)).  i 

Friedreich**  Hereditary  Ataxia.  (flBl.  170)  i 

DiMeminnted  Sclerosis,  (086.  7ft<ll.  ' 

Cerebral  Disease  (especially  of  the  brain  stem),  ' 

Spasmus  Nutans,    Nktitatio  Spastica.  (679).  ' 

X.vatairmns-myoclonut. 

Ocular   Muscular  Insufficiency.    (81S).      (Pijw,  14, 

Svfingomyelia.  (.WS.  840  2,  1000.  11.52.  1170.  11R7. 

11170.21.     iVle*.  25-7). 
Chronic  Bulbar  Paralysis.  (61S,  lir.l).  (FHe»-  21-2). 

.Vmyotrophii-  I.uteral  Sclcrosi..  (MT.  SIMI.  lirrf».  ' 

(t^gs.  24-6). 
Spinal  or  Neuritlc  Muscular  .Mrophy,  (40r.). 

Myokymia,     Myoelonio,  (204).  ' 


O 


CHART  XIIc 
Local  Palsies 

Comprising  Numbers  700  to  721  on  right  margin. 


(Note) — The  anesthesia  accompanying  these  palsies  can  be  seen  from  the  areas  of  cutaneous 
distribution  of  these  nerves  depicted  in  the  plates  at  the  end  of  the  book  (Figs.  33-8).  In  mild 
lesions  of  the  nerves  anesthesia  is  either  absent  or  much  less  marked  and  less  extensive  than 
is  the  motor  paralysis. 


155 


DIAGNOSTIC  ANALYSIS  OF   SYMPTOMS 


Inabiuty  to 
Move,  more 

OR   LESS, 

Muscles 

THE 


LOCAL  PALSIES 
Abstract  of  Symptoms 


OF 


E 
Y 
E 
B 
A 
L 
L 


J 
A 
W 


P 

A 
G 
E 


'  There  are  ptosis  and  strabismus  divergens  and  the  pupil  is  dilated 
and  immobile  both  to  light  and  accommodation  (this  condition  of 
the  pupil  may  occur  as  an  isolated  paralysis, — 333)-  The  eye- 
ball can  be  moved  in  no  direction  except  outward  (abducens), 
and  outward  and  downward  with  rotation  of  eyeball  (superior 
obUque).  For  symptoms  characteristic  of  the  isolated  paralysis 
of  each  ocular  muscle  see  Chart  XIVc,  818.  When  the  superior 
oblique  muscle  is  paralysed  by  an  intra^orbital  lesion  the  levator 
paJpebrae  superioris  is  usually  paralysed  with  it  and  ptosis  re- 
sults. 

The  ocular  muscles,  except  the  levator  palpebrae  superioris,  have 
a  bilateral  cortical  representation.  Hence  ocular  paralyses, 
except  ptosis,  almost  never  occur  in  lesions  above  the  oculo- 
motor nucleus,  except  in  bilateral  lesions.  The  cortical  repre- 
sentation of  the  ocular  muscles  seems  to  be  very  diffuse  or 
multiple.  Conjugate  deviation  may  result  from  supra-nuclear 
lesions. 

For  the  symptoms  of  paralysis  of  the  trochlearis  (patheticus) 
nerve  and  of  the  abducens  nerve,  each  of  which  produces  a 
strabismus  convergens,  see  818. 

r  The  muscles  of  mastication  of  one  side,  rarely  of  both  sides,  are 
paralysed  and  in  severe  cases  atrophied.  The  temporal  and 
masseter  muscles  cannot  be  felt  firmly  contracting  when  eiTorts 
are  made  to  chew.  The  jaw  cannot  be  closed  tightly  or  opened 
strongly  or  moved  laterally  towards  the  healthy  side  (external 
pterygoids),  or  the  chin  pushed  forwards  (internal  pterygoids). 
Mastication  of  food  is  difficult  or  impossible;  dysmasesis 
(286).  The  jaw  reflex  (323)  is  abolished.  In  some  cases  one 
side  of  the  soft  palate  (tensor  veli  palatini)  is  paralysed  and  in 
some  the  hearing  of  low  tones  is  unpleasant  (tensor  tympani). 

In  trigeminus  lesions  there  is  unilateral  abolition  of  the  con- 
junctival, corneal,  sneezing  and  palatal  reflexes;  and  the 
secretion  of  tears  is  at  times  affected.  There  is  no  irritation,  or 
tears,  from  inhaling  ammonia  or  acetic  acid.  There  is  also  loss 
of  sense  of  taste,  dilation  of  the  pupil,  narrowing  of  the 
eyelid  slit  and  even  enophthalamos.  Heat  and  redness 
of  skin  in  recent  cases  and  coldness  and  cyanosis  of  skin  in  old 
cases.  The  salivary  secretion  and  taste  are  affected  when  either 
the  proximal  or  the  distal  end,  but  not  the  middle,  of  the  nerve 
is  affected- 

The  muscles  of  expression  of  one  side  (facial  monoplegia), 
rarely  of  both  sides,  (facial  diplegia)  n£  the  face  are  paralysed. 
The  forehead  cannot  be  wrinkled  and  the  eye  appears  larger  than 
normal  and  cannot  be  closed  (lagophthalmos,  hare's  eye). 
When  attempts  are  made  to  close  the  eyelids  the  eyeball  turns 
upward,  the  cornea  disappearing  behind  the  upper  lid  (Bell's 
phenomenon — 434).  The  angle  of  the  mouth  is  lower  than  nor- 
mal and  cannot  be  rai.sed.  The  naso-labial  fold  is  obliterated. 
The  lips  cannot  be  firmly  closed ;  so  that  whistling  is  impossible 
and  speech  is  impaired.  Mastication  is  difficult,  because  the 
weakened  buccinator  muscle  allows  food  to  collect  between  the 
jaws  and  the  cheek.  The  platysma  is  also  paralysed ;  so  that 
the  angle  of  the  mouth  cannot  be  drawn  downwards.  Tears 
may  flow  from  the  eye  and  irritate  the  cheek  and  saliva  from 


Diagnosis 

Paralysis  700 
of  Motor 
Oculi. 
(Figs.  14,  18). 


Paralysis  701 
of  Troch- 
learis and 
of  Abducens. 

Paralysis  702 
of  motor 
branch  of 
Trigeminus. 


Facial 

Paralysis. 

Bell's 

palsy. 

Prosopo- 

plegia. 

Facial 

Monoplegia. 

Facial 

Diplegia, 

(751,^928, 

1333). 


703 


156 


LOCAL  PALSIES  (Continued) 


Inability  to 
Move,  more 

OR  LESS, 

Muscles  of 

THE 


F 
A 
G 
E 


G 
o 
n 


P 
H 
A 
R 
Y 
N 
X 


Abstract  of  Symptoms  Diagnosis 

the  angle  of  the  mouth.  The  conjunctiva  may  become  inflamed 
and  the  cornea  ulcerated,  because  the  eyelid  cannot  wink  and 
keep  the  conjunctiva  clean.  In  some  cases  the  facial  paralysis 
may  be  preceded  and  accompanied  by  pain.  When  both  sides 
of  the  face  are  paralysed  (facial  diplegia)  the  symptoms,  just 
described,  are  present  on  both  sides.  This  condition  is  not  quite 
so  easily  recognized,  because  there  is  no  healthy  side  to  com- 
pare and  contrast  with  the  paralysed  one.  In  severe  cases  the 
paralysed  muscles  exhibit  the  electrical  reaction  of  degeneration. 
Hearing  and  taste  are  frequently  impaired  and  disordered. 
When  taste  is  affected  the  salivary  secretion  is  also  affected. 
In  the  early  stages  of  the  disease  the  face  is  drawn  over  toward 
the  healthy  side  by  the  unantagonized  healthy  muscles.  In  the 
later  stages  the  face  may  be  drawn  back  again  permanently  to- 
wards the  paralyzed  side  by  the  contracting,  newly  formed  con- 
nective tissue  in  the  degenerated  muscles.  Also  in  the  early 
stage  of  recovery  the  face  may  be  drawn  towards  the  paralyzed 
side  by  over-innervation  of  the  muscles  formerly  paralyzed,  and 
may  exhibit  temporary  contractures  and  spasms,  possibly  "as- 
sociated movements."  These  spastic  symptoms  may  be  due  to 
irregular  regeneration  of  the  nerve-  The  upper  fibres  of  the 
facial  nerve  have  a  bilateral  cortical  representation  as  do  the 
laryngeal  nerves.  Hence  lesions  of  the  cerebral  hemispheres 
paralyse  mainly  the  lower  branch  of  the  facial ;  the  eye 
on  the  paralysed  side  can  be  closed,  but  is  easily  forced  open. 
For  the  localization  of  the  different  forms  of  facial  paralysis, 
see  1333. 


The   glosso-pharyngeus   nerve   contains  motor  as  well  as  sensory  Glosso-    703a 

fibers  and  lesions  of  it,  probably,  cause  partial  or  complete  para-  pharyngeus 

lysis  of  the  pharnyx ;  but  no  isolated  lesion  of  the  glosso-pharyn-  Paralysis 
geus  has  been  recorded. 


L 
A 
R 
Y 

N 
X 


N 
£ 
G 
K 


Paralysis  of  the  pneumogastric  nerve  is  discussed  under  763.  In 
addition  to  the  laryngeal  paralysis  there  are  often  present  dis- 
order of  the  respiratory  act  and  of  the  heart  beat  (tachycardia) 
and  unilateral  paralysis  of  the  soft  palate. 


,  When  the  tip  of  the  shoulder  sinks  downwards  and  forwards  and 
the  arm  cannot  be  easily  raised,  there  may  be  a  paresis  of  the 
trapezoid  muscle.  When  tliis  muscle  is  paralysed  on  both  sides, 
the  head  tends  to  fall  forward.  When  the  head  is  drawn  towards 
one  shoulder  and  the  chin  turned  upwards  and  towards  the  other, 
the  sterno-cleido-mastoid  muscle  is  paralysed  on  that  side 
toward  which  the  chin  turns.  This  posture  is  called  caput  obsti- 
pum  .spasticum,  when  the  muscle  is  atrophied  and  secondarily 
contracted  and  the  deformity  can  no  longer  be  corrected  by 
passive  motion.  Caput  obstipum  spasticum  occurs  also  and  is 
more  pronoimced  in  torticollis  from  spasm  of  the  muscle  (730). 
When  the  sterno-cleido-mastoid  muscle  is  paralysed  on  both 
sides,  the  head  tends  to  fall  backwards. 

r  When  one  side  of  the  tongue  is  paralysed,  as  frequently  happens 
I  in  hemiplegia,  the  tongue  when  protruded  turns  towards  the 
I      paralysed  side.     When  both  sides  are  paralysed  the  tongue  can- 


Pneumo-  704 
gastric 
Paralysis 
(760). 


Paralysis  705 
of  the 
Spinal 
Accessory. 


157 


LOCAL  PALSIES  (Continued) 


Inability  to 

Max's,    MORE 
OR  LESS, 

Muscles  of 

THE 

T 
0 
N 
G 
U 
E 


D 
I 
A 
P 
H 
R 
A 
G 
M 


Abstract  of  Symptoms 

not  be  protruded  at  all,  and  in  such  cases,  speech,  mastication 
and  deglutition  are  difficult  and  imperfect.  In  lesions  of  the 
nucleus  of  the  hypoglossus  nerve  there  is  a  paralysis,  usually 
bilateral,  associated  with  patches  of  muscular  atrophy  and  with 
tremor.  There  are  often  also  paralysis  and  atrophy  in  groups  of 
muscles  in  the  hands  and  shoulders  (Progressive  muscular 
atrophy — 546 ) .  There  is  also  a  mild  paresis  of  the  orbicularis 
oris  muscle.  Intracranial  lesions  involving  the  hypoglossus  and 
other  nerve  roots  at  the  base  of  the  brain  may  cause  Ave  His' 
syndrome:  pharyngo-laryngeal  or  glosso-pharyngo-laryngeal 
paralysis  combined  with  paralysis  of  the  soft  palate  and,  if  the 
hypoglossus  nucleus  be  involved,  of  one-half  of  the  tongue 
also ;  or  may  cause  Schmidt's  syndrome :  the  above  and  also 
stemo-cleiido-niastoid  and  trapezius  paralysis*  In  lesions  of 
the  cortical  hypoglossus  area,  even  unilateral  ones,  a  bilateral 
paralvsis  of  the  tongue  may  result,  without  atrophy  and  without 
any  change  in  its  electrical  reactions. 


The  diaphragm  is  paralysed  on  one  or  both  sides,  causing  dyspnoea 
on  exertion  and  sinking  in  of  the  epigastrium  on  inspiration, 
especially  on  deep  inspiration.  The  lower  part  of  the  lung  is 
drawn  upwards  and  atolectasis  and  pneumonia  may  occur.  Be- 
sides the  usual  causes  of  compression  and  neuritis,  this  paralysis 
may  also  occur  in  pleurisy,  peritonitis,  trichinosis  and  in  bulbar 
and  spinal  lesions.  The  paralysed  diaphragm  shows  Litten's 
phenomenon. 


Diagnosis 


Hypo- 
glossus 
Paralvsis. 
(546,' 755) 


706 


Phrenic       707 
Paralysis. 


A 
R 
M 


The  supra  and  infra-spinatus  muscles  are  paralysed;  so  that  rota- 
tion of  the  arm  outward  and  raising  it  in  abduction  are  impaired. 
Muscles  involved  are  atrophic  and  ulnar  side  of  hand  is  turned 
forwards. 

The  serratus  anticus  major  is  paralysed:  so  that  when  the  scapula 
is  raised,  its  lower  angle  approaches  the  vertebrae  and  the  inner 
margin  of  the  scapula  does  not  lie  close  to  the  thorax  and.  on 
movements  of  the  arm  upwards  and  forwards,  stands  from  the 
thora.x  like  a  wing.  The  arm  cannot  be  raised  beyond  a  hori- 
zontal line. 


Supra-         708 

.Scapular 

Paralysis. 

Long  709 

Thoracic 

Paralysis. 

Serratus 

Paralvsis. 


Motion  of  the  arm  inward  and  forward  is  impaired. 
Hand  cannot  he  placed  on  opposite  shoulder. 


.interior  and  Posterior  710 
Thoracic  Paralvsis. 


Rotation  of  the  arm  inward  and  motion  of  the  arm  backward 
are  impaired. 


Sub-Scapular  71 1 
Paralvsis. 


The  deltoid  and  teres  minor  are  paralysed:  .so  that  the  arm  can-    .A.xillary       712 
not  be  raised.  Paralysis. 

The  combined  paralyses  of  the  brachial  plexus :  Erb's  and  Klump- 
ke's  paralysis,  are  discussed  under  444,  445  and  490. 


The  biceps,  brachialis  anticus    and    coraco-brachialis    muscles  are  Musculo- 

more  or  less  completely  paralysed;  so  that  flexion  of  the  arm  at  Cutaneous 

elbow  is  more  or  less  impaired,  especially  in  supination   (very  Paralysis, 
rare.) 


71.3 


158 


LOCAL  PALSIES  (Concluded) 


Inability  to 
Move,  more 
OR  Less, 
Muscles  of 

THE 


H 
A 
N 
D 


E 
G 


Abstract  of  Symptoms 

The  pronators  and  flexors  of  the  hands  and  fingers,  the  muscles  of 
the  ball  of  the  thumb  and  the  first  and  second  lumbrical  muscles 
are  paralysed.  The  hand  can  neither  be  flexed  nor  pronated- 
The  thumb  cannot  be  brought  across  the  hand  to  touch  the  little 
finger,  but  remains  close  to  the  index  finger  (ape's  handj.  The 
first  (proximal)  phalanges  of  fingers  can  be  flexed,  but  not  the 
second  and  third  phalanges. 

The  interossei,  the  third  and  fourth  lumbricales,  and  the  muscles 
of  the  little  finger  are  paralysed.  The  proximal  phalanges  can- 
not be  flexed,  the  other  phalanges  cannot  be  extended  and  the 
J  little  finger  cannot  be  moved.  The  fingers  cannot  be  spread. 
When  muscle  atrophy  and  contracture  occur  "claw  hand"  re- 
sults. 

The  extensors  and  supinators  of  the  hand  and  fingers  and  the  ab- 
ductor pollicis  longus  are  paralysed.  The  thumb  is  adducted 
and  can  neither  be  abducted  nor  extended.  Wrist-drop  and 
slight  pronation.  Wrist  and  fingers  cannot  be  extended  com- 
pletely. The  wrist-drop  differs  from  that  of  lead  palsy  (494) 
in  that  the  supinator  longus  is  paralysed.  Therefore,  if  the 
forearm  is  held  midway  between  supination  and  pronation  and 
the  elbow  strongly  flexed  against  a  resistance  offered,  the  belly 
of  the  supinator  longus  will  not  stand  out  firmly  contracted  as 
it  will  in  lead  paralysis  and  in  health. 

•  The  extensor  femoris  is  paralj'sed ;  so  that  flexion  of  the  thigh 
on  the  body  and  extension  of  leg  on  thigh  are  impossible  or 
difficult.  Standing  and  walking  are  difficult,  and  ascension, 
jumping  and  running  impossible.     Knee-jerk  usually  absent. 

The  adductor  muscles  of  thigh  are  paralysed;  so  that  adduction 
of  leg,  pressing  of  thighs  together  and  crossing  of  legs  are  im- 
possible. 

The  glutei  muscles  are  paralysed ;  so  that  walking,  ascending 
stairs,  straightening  up  of  body,  abduction  and  rotation  of 
thigh  are  impaired.     Generally  much  muscular  atrophy. 

Foot  and  toes  are  paralysed ;  the  leg  cannot  be  flexed  at  knee  and 
rotation  of  the  thigh  is  impaired.  In  cases  of  isolated  tibialis 
paralysis  there  is  absence  of  plantar  flexion  of  foot,  and  of 
plantar  flexion,  spreading  and  adduction  of  toes  (Pes  calcaneus 
et  valgus.)  In  cases  of  isolated  peroneal  paralysis  there  is 
absence  of  dorsal  flexion  and  abduction  of  foot  and  its  adduc- 
tion impaired — absence  of  dorsal  flexion  of  toes.  There  are 
foot-drop,  high  stepping  gait  and  Pes  equino-varus. 


For  paralysis  from  lesions  of  the  cauda-equina,  see  487,  1007  and 
1308. 


Diagnosis 

Median     714 
Paralysis. 


Ulnar     715 
Paralysis. 


Musculo-  716 
Spiral  and 
Radial 
Paralysis. 


Crural       717 

Paralysis 

(997). 


Obturator  718 
Paralvsis. 


Gluteal       719 
Paralysis. 


Sciatic,      720 
Tibial  and 
Peroneal 
Paralysis. 
(996). 


Cauda 
Equina 
Paralysis. 
(Fig.  29). 


721 


159 


CHART  Xlld 
Local  Spasms 

Comprising  Numbers  725  to  733  on  right  margin. 


161 


Spasm  of 
Muscles  of 

E 
Y 

E 


J 
A 
W 


P 
A 
C 
E 


P 
H 
A 
R 
Y 
N 
X 


L 
A 
R 
Y 
N 
X 


DIAGNOSTIC  ANALYSIS  OF  SYMPTOMS 

637— LOCAL  SPASMS 

Abstract  of  Symptoms  Diagnosis 

f 

\  For  spasm  of  ocular  muscles,  see  XIV,  878. 
I 

I 

r  The  jaws  are  held  tightly  shut  and  the  masseter  and  temporal  mus-      Trige-  725 

I       cles  can  be  felt  to  be  contracted  (lock  jaw),  usually  bilaterally,      minal 
The  spasm  may  be  "tonic,"  as  in  tetanus  (603),  tetany  (612),      Spasm  or 
irritation  of  teeth  (wisdom  teeth)  and  certain  unilateral  lesions      Cramp, 
of  the  pons  and  medulla;  or  "clonic,"  as  in  chills  and  in  rare      Trismus, 
cases  of  paralysis  agitans  and  hysteria.     When  the  pterygoid 
muscles  alone  are  in  spasm  the  mouth  is  held  open  and  cannot 
be  closed. 

Spasms  of  one  or  more  muscles  of  expression  of  the  face,  uni-      Facial  726 

lateral  or  bilateral,  are  relatively  common,  as  in  convulsive  tic  Spasm  or 
(598)  and  tic  douloureux  (599).  These  spasms  are  often  a  Cramp 
mixture  of  tonic  and  clonic  contractions,  the  clonic  predomina-  (267,  598-9). 
ting.  They  may  affect  all  the  muscles  or  only  one,  as  in  tonic 
spasm  of  the  orbicularis  palpebrarum  (blepharospasm)  (598, 
616),  or  in  clonic  spasm  of  this  muscle  (spasmus  nictitans: 
nictitation).  The  platysma  niyoides  often  takes  part  in  these 
spasms  and  very  rarely  the  muscles  of  the  soft  palate  and  the 
internal  and  external  ear  muscles.  Very  rarely  spasm  of  some 
of  the  facial  muscles  about  the  mouth  constitutes  an  occupation 
neuro.sis  or  cramp,  as  in  the  "Auctioneer's  cramp"  and  "Comet 
player's  cramp."  These  facial  cramps  may  be  symptomatic  di- 
rectly of  lesions  of  the  cortical  facial  center,  of  the  facial  nerve 
in  its  course,  and  reflexly  of  the  trigeminal  nerve  or  its  terminal 
filaments  in  the  eye,  nose,  mouth  or  ear.  There  are  also  to  be  re- 
membered the  passive  contracture  of  the  degenerated  muscles 
and  the  active  contracture  due  to  over-innervation  of  the  con- 
valescing muscles  in  facial  paralysis.  Causeless  and  uncon- 
trollable laughter  must  also  be  classed  among  the  facial  spasms. 
This  condition,  similar  to  the  allied  state  of  causeless  and  un- 
controllable crying,  occurs  especially  in  hysteria  and  in  lesions 
of  the  optic  thalamus. 

Spasm  of  the  pharynx  of  a  tonic  nature  preventing  swallowing  and      Glosso-     727 
of  a  clonic  nature  repeating  the  act  of  swallowing  with  great  fre-      pharyn- 
quency  occur-     The  former  occurs  in  hydrophobia  (604)   and      geal 
somewhat  also  in  tetanus  (603)  :  while  the  latter,  as.sociated  with      Spasm  or 
coma,  frequently  occurs  in  mild  epileptic  attacks.     The  sjjasm      Cramp, 
also  occurs  from  irritation  of  the  pharynx  in  hysteria  and  very 
rarely,  as  one  of  the  crises  in  locomotor  ataxia  (423).     Spasm 
of   the   oesphagus   is    not  uncommon  in  hysterical  persons  and 
makes  the  swallowing  of  food  very  difficult. 

Spasm  of  the  muscles  of  the  larynx  (.spasmus  glottidis,  false  croup,      Pneumo-     728 
laryngismus  stridulus),  causing  noisy  and  difficult  breathing,  is      gastric 
a  not  uncommon  and  occasionally  a  dangerous  condition.     It      Spasm 
occurs  almost  exclusively  in  children    and    is   often    associated      or  Cramp, 
with    rickets    and    with    digestive    disorders.     Occurs    also    in 
general  diseases  such  as  hydronhobia,  hysteria,  epilepsy,  chorea, 
tabetic   crises,   etc.      Sneezing    (sternutatio    spastica,   ptarmus) 
and  coughing,  reflex  acts  implicating    both    the    pneumoga.stric 
and  the  intercostal  nerves,  are  often  due  to  pathological  con- 
ditions   and    irritation    of    the    nervous  system.     Bradycardia, 
Cheyne-Stokes'  respiration  and  cerebral  vomiting  are  symptoms 
of  irritation  of  the  pneumogastric   nucleus,  but  are  not  charac- 
teri.stic  and  are  of  little  diagnostic  value. 


162 


Spasm  of 
Muscles  of 


T 
0 
N 
G 
U 
E 


N 

E 
C 
K 


D 
I 
A 
P 
H 
R 
A 
G 
M 

A 
B 
D 
0 
M 
E 
N 

A 
R 
U 


L 
E 
G 


LOCAL  SPASMS   (Continued) 

Abstract  of  Symptoms 

-  Spasm  of  the  tongue  is  very  rare,  especially  so  the  tonic  form. 
During  the  attack  speaking  and  swallowing  are  impossible.  Very 
rarely  a  tonic  spasm  of  the  tongue  occurs  when  the  patient  at- 
tempts to  speak  (stuttering  and  aphthongia).  Spasm  of  the 
tongue  is  sometimes  associated  with  facial  spasm  and  with  spasm 
fo  the  submaxillary  muscles.  These  spasms  may  be  due  di- 
rectly to  lesions  of  the  cortical  tongue  center,  of  the  hypoglossus 
nerve  in  its  course,  or,  refiexly,  especially  from  lesions  of  teeth, 
mouth  and  nose. 


r  Spasm  of  the  neck  muscles,  especially  the  stenio-cleido-mastoid, 
caput  obstipum  ( spastic  wry  neck ) ,  is  sometimes  congenital  and 
is  sometimes  acquired  in  later  life.  In  these  cases  the  head  is 
drawn  toward  the  shoulder  of  the  affected  side  and  the  chin  is 
turned  toward  the  other  side  and  slightly  elevated  and  the 
stemo-cleido-mastoid  muscle  can  be  felt  to  be  firmly  contracted. 
When  the  trapezius  is  the  seat  of  the  spasm  the  occiput  is  drawn 
backwards  and  turned  toward  the  shoulder  of  the  affected  side 
and  the  edge  of  the  muscle  can  be  felt  to  be  firmly  contracted. 
Spasm  of  the  muscles  is  sometimes  tonic,  sometimes  clonic  and 
often  both.  The  cause  of  these  spasms  is  often  neurotic  and 
often  rheumatic.  Rarely  it  is  some  disease  of  the  eye  or  of  the 
ear  (torticollis  ab  oculo  laeso,  ab  aure  laesa)  or  of  the  cervical 
vertebrae.  Usually  many  muscles  are  involved,  although  one  or 
two  more  prominently  than  the  others.  Spasm  of  the  neck 
muscles  with  retraction  of  the  head  is  a  prominent  symptom  in 
meningitis  and  strychnine  poisoning. 

Tonic  spasm  of  the  diaphragm,  either  unilateral  or  bilateral,  occurs 
very  rarely  and  produces  dangerous  dyspnoea.  It  sometimes 
occurs  as  one  symptom  of  a  general  disease:  tetanus,  hydro- 
phobia, hysteria,  etc.  Clonic  contractions  are  common  and 
cause  hiccough  (singultus),  always  a  distressing  and  at  times  a 
dangerous  symptom,  which  occurs  occasionally  in  brain  and 
spinal  cord  lesions  and  frequently  in  irritation  of  the  pneu- 
mo^stric  nerve,  especially  from  the  gastric  mucous  membrane. 
A  similar  but  slower  contraction  of  the  diaphragm  associated 
with  facial  spasm  (opening  of  mouth)  causes  the  act  of  yawn- 
ing (oscedo,  chasmus)  which  is  sometimes  frequently  repeated 
as  an  aura  of  apoplexy  or  epilepsy  and  occurs  also  in  hysteria, 
digestive  disorders,  drowsiness,  etc. 

f  Tonic  and  clonic  contractions  of  some  or  all  of  the  abdominal  mus- 
I  cles  occur  with  extreme  rarity,  and  the  latter  are  usually,  if  not 
always,  hysterical.  Rigidity  and  retraction  of  the  abdomen  oc- 
cur in  meningitis,  peritonitis  and  in  perforation  of  stomach  or 
bowels.  Local  or  general  rigidity  occurs  in  appendicitis,  rupture 
of  the  Fallopian  tube  and  the  varous  colics. 

Tonic  and  clonic  spasms  of  the  muscles  of  the  arm  and  shoulder 
or  of  the  leg,  with  the  exception  of  the  secondary  contractures 
due  to  lesions  of  the  pyramidal  tract  and  of  the  peripheral 
nerves,  are  very  rare.  They  usually  are  due  either  to  deficiency 
of  water  in  the  system,  and  often  occur  in  disease  in  which 
much  water  is  lost,  as  cholera,  diarrhoea,  etc-,  or  to  hysteria,  or 
to  rheumatic  factors,  or  are  reflex.  The  deformity  resulting  in 
each  case  can  be  predicted  from  the  function  of  the  muscle 
involved. 


Diagnosis 

Hypo-       729 
glossus 
Spasm  or 
Cramp. 
(770-1). 


Spinal        730 
Accessory 
Spasm  or 
Cramp 
(598). 


Phrenic     731 
Spasm  or 
Cramp. 


Inter-        732 

costal 

Sf)asm. 

Abdominal 

Spasm. 


Brachial,  733 
or  Lumbar, 
or  Sciatic 
Plexus, 
Spasm  or 
Cramp. 


163 


CHART  XIII 


Disorders  of  Speech  and  Gait 


DIAGNOSITIC  ANALYSIS  OF  SYMPTOMS 


Symptoms 
Analysed 


735 

DISORDERS 

OF  SPEECH, 

READING 

AND 

WRITING. 


Character  of  Disorder 


nz7 


"I 


ANARTHRIA  (283) 

Inability  or  unwillingness  to  speak.  No 
disease  of  vocal  organs  or  peripheral 
nerves.  This  condition  may  result  from 
a   complete   aphonia    (260)    or  complete 


The  diseases   in   which  Anarthria 


aphasia     (222)    or   complete    dysarthria  l  ,        ,    Dvsarthria   occur    are    -^et 
(09.±\    «^ /i»i„=;rKr,c  /'1119^    r.T- H«nmnfi'a  I      auQ   ijysarmna   occur   are    sei 


(284),  or  delusions  (1112),  or  dementia 
(1095),  or  voluntarily. 

738 

DYSARTHRIA  (284) 
Ability   to   express    thought  by  speech  but 
articulation  is  defective. 

739 

APHASIA  (222  to  233) 
Articulation  normal  but  expression  of  nor- 
mal thought  is  defective. 


forth  in  Chart  Xllla. 


The  varieties  of  Aphasia  and  the 
conditions    under    which    they 
occur       are     set       forth      in 
Chart  Xlllb. 


736 

DISORDERS 
OF  GAIT. 


r740 
ATAXIC 

741 

PARALYTIC  AND  FLACCID 

742 

PARALYTIC  AND  SPASTIC 


The  diseases  in  which  Disorders 
of  Gait  occur  are  set  forth  in 
Chart  XIIIc. 


165 


CHART  Xllla 

Anarthria  and  Dysarthria 

Comprising  Numbers  Thl  and  738  on  left  side  of  Chart 
and  743  to  771  on  right  margin 


167 


o 


DIAGNOSTIC    SYMPTOMS    AND    TESTS 


DIAGNOSTIC   ANALYSIS   OF   SYMPTOMS 
ABSTHACT   OF   SYMPTOMS 


BMult  ol  diieue  ia 

Auditory  nifuii^rk-s 

int^BCj,  or  cooecd- 

ipokei)   words  w 

iUL 

lodi  tlirojgb  diSM 

rii-j)      iieci^urj- 

3veeMary  for  uQdentandinK    fMa>   lunkr 
e  never  acquired,  or  esrlr    j 
!<■:  buDce  iDnerratioD  memo    "j  ,,  _    ,_ 
(or     spcetb      were     never  " 


aU'lit. 


noise  but  i-uuQOC  apeak, 
.imnj  to  speak  tbrough   the  j 


1401)' 


looervutJoD  inemories  uecvssarj  for  apeccb 
bave  been  acquirml  but  are  not  available.  No 
bysterical  *ymploin». 

llyatericAl  (ymjitouu  aud  enolo^ical  fsctots 
l>r««eat,  Altbougb  not  alwoya  promioeDt. 


Complete  absence  of  speech,  and  readiog  altad 
ii    impnssiblv.      Pnticnt    maKes    do    effort 
speak  or  lo  coiumuuicate  by  ueature^. 


ion  of  face  and  actions  are  idiotic. 
iuD  of  face  and  notions  ore  normal. 
Abseiioe  of  facial  expression  and  of  ail  volun 

UCtiOQB, 

exprension  and  BCtions  are  abnormal. 


Reading    and    writing 
after  mucb  traininf. 


Paiic&i  L-xhibits  littie  or  no  intelligence  and  history  shows  that  be  never  bad  any.    Incapable  o( 
any  but  the  moat  elementary  education,  if  of  any.     Soils  himself  with  ucine  and  feces. 

PaticDt  shon'8  a  good  intellieence,  but  can  expreK  himself  only  hy  eeatures  and  tbat  only  aa  ttaa 
result  of  careful  training.    Some  deaf  muteacao  be  taught  to  speak,  eener&lly  Tery  imperfectly. 


ud    j-Absenc 
to  \      lary 


in  a  deep  sleep  and  cannot  be  aroused  to  any  expression  of 


r  intelligeoce  by  stimulation  of  any  sensory  surface. 


ilient  is  evidently  insane  and  has  delusions.     When  recovery  has  taken   place  it  may  be  lenraed   that  bis  silence  was  due  to  a  delusion, 
usually  either  of  fear  or  of  a  divine  command  (delusional  insanity). 


Hysl 


si]  appearance.    Placid  and  ctntentcd. 


■\naribria 
fl'robnbly  only  a  severe  form  of  hr«erical  aphonia.     It  is  a  rare  condition. 
[Ciin,  by  hard  urging,  be  made  to  whisper  some  words  faintly  but  distinctly 


I  profound  dementia. 


Idiocy.   (10S3). 

Deaf  MuQtdu. 

Coma.   (205.  1037). 
Insanity,  (1041). 


Apoplectic  symi'tiimn 

\'ocftl  orsauB  defectlv 
Vocal  organs  nnnnol. 


Will  neither  wbiaper  nor  speak. 

Can  whisper  faintly  but  distinctly.  j 

Mny  mutter  but  cannot  articulate  distincQj;     Sudden  imsct,  usually  followed  by  speed.v  death.    Paralysis  of  motion  or  sensation  or  of  both  in  the  extremities. 

Loss  of  speech  may  be  complete  or  patient  ^yln-  ublp  to  ssy  one  or  two  words  distinctly.     There  may.  or  may  not  be,  paralysis  of  motion,  ot    sensation,  or  of  both  in  the  eilremities. 

Wi>ids  imperfectly  formed,  also  a  nusai  voice.     An  exatfbltionof  the  vocal  organs  shows  no  paralysis,  but  a  developmental  d'->fe<'t :  such  its  deft  palate  and  «mitar  malformation. 

U'urds  imperfectly  formed  and  usually  a  very  limited  nhbulsry-     Intelliuence  very  defective.     Paralysis,  usually  of  the  spaati'-  variety,  may  be  present  in  tbe  extremides. 

Siilisiitution  of  one  letter  for  another.    An  exnniinaiioa  gt  the  vucal  organs  shows  no  defects  or  parnlyais.     Patients  exhibit  a  nither  childish  or  affe<^ied  form  of  9ijee<<h.    Some  subsitute  "W  tor  "R",  others  use  "TH" 
^jifaks  tbe  vowels  correctly  but  liaa  difficulty  in  speftlfcs  certain  consouiinis  and  substitutes  otliers  for  them :  thus  apparenily  invents  a  ni*w  language.   This  speech  usually  becomes  normal  js  Ihr  child  gmws  older. 


1  few  woTil*.  nysteiioil  Mutism,    (lOT'Jl. 

Hysterical  Aphonia.  (762,  107«). 
Apoplexy  in  pons  or  medulla. 
Destruction  of  Cortical  Motor  Speech  Ccnt«r 
Cleft  Palate,  etc. 
Imhedlity,  (lOGO). 
In  idio^lo»sln  a  child      Lisping  and  Lalling  and  Idloglossia. 


Patient  cannot  whistle  or  ciose  lips  ti?btly. 
Tongue  la  not  protruded  straight  but  deriatcs 


t  be  clearly  spoken,  especially  when  the  paralysis  is  bilateral. 


Soft  palate  is  sot  raised  (bilateral)  < 


.\ne<(tbesia  of  larynx.    Paralysis  ot  ctico-tbyroid  musdi  (vit-al 
and  on  lower  level)  aod  of  thy reo-ar}-epi glottis  musdl  (epi^li 


panlysi)  side,  or  cannot  be  pimtruded  at  all. 

1 

not  raised  synimfri cully  (unilateral)   in  pbonation. 
lOt  tense  in  pboi 


iMbiiity  of  one  or  both  vocal  cords  from  paralysis  of  |tn 
■lie  pnsjiioD  of  cords   (between  extreme  adduction  a£ 

cases  of  unilatemi  paralyaiB.  the  healthv  cir-t  moift  acr^> 
iralysed  cord. 


.ill  tbe  laryngeal  muscles.    Cada- 

reme  abduction).     In  phonatlon, 

median  line  to  reach  the 


LinRuals  cannot  be  clearly  spoken.     This  dlGBoulty  is  usually  temporary.     Nasal   voice. 
Liquids  may  regurgitate  through  nose. 

Nasal  voice.    Indistinct  articulation,  which  ia  improved  when  head  is  thrown  backwards. 

Voice  bourse.     In  swallowing,  larynx  is  not  well  closed;  so  timt  food  enters  it,  causing 
cough,  dyspnoea  and  possibly  deglulitioQ  pneumonia. 


Aplionia.  weak  cough  and  snoring  breathing  if  bilateral. 
Weak,  hoarse  voice  if  unilateral.  If  bilateral  the  cords 
are  ducktd  together  during  inspiration,  giving  rise  to  a 
slight  stridor. 


Other  fuHal  muscles  are  paralysed. 

May  he  evidence  of  injury  or  pressure  upon  bypoglossus  netre. 

May  follow  dipbtberia.    Liquids  may  regurgitate  through  note. 
May  foHow  dipbtberia. 


Paralysis  of  Poeial  nerve.  (708.  ftSS.  1383). 
Paralysis  of  Hypoglossus  nervf.    (TOtf). 

Paralysis  of  Levator  Palatl. 
Paral.vsjs  of  Superior  Laryngeal  N"er%'e. 


irl'^- 


The  labials,  the 
linptols  or  tbe 
vowel  Ronndi  or 
nil  of  them  cannot 
he  properly  pro- 
nounred.  A  care- 
ful exnmlnntion  r^- 
veJil*  a  parnlysli 
or  n  paresris  within  , 
the  drimsin  of  tlie 
fncial.  the  hypo- 
Slo^ttl  or  tie 
pne  ti  m  0  g  a  s  t  i  c 


1(1  111  MUf  ur  both  vocal  cords  from  paraiysi?  ofcnoi 
>r  cords  lie  near  the  median  line  (extreme  nidation 
r  ■mailer  on  Inspiration. 


of  one  or  both  vocal  coi-ds  from  pnrnlysi 
<i  Iiiieralis  musolm  and  in  «ome  cate^  the  i 
I  litnt'i".   Cords  are  wld^  open  (ahdnctlou) 


■  rytenoid  posterior  muscle.     The 
leaving  narrow  alit  which  may 


Voice  very  little  altered.  If 
bilateral,  there  is  great 
inspiratory  dyspnoea  with 
stridor. 


rumor  or  lesion    alone  course   of.   or      Paralysis  of  the  entire  Recurrent  l-aryngeal  Nen.e 
in.  recurrent  laryngeal  neire,  eape-  (Recurrens  Pnmlyits). 

daily  lesions  of  the  aorta  or  lungs. 


May  he  tumor  or  lesion  along  the  recurrent  u.?rve.     May  be  Parslysis  of  Crico- Arytenoid  Posterior  Nerv 
the  first  symptom  of  an  entire   recurrent   paralysis,   or  one  (.ibductor  or  Posticus  Paralysis). 

symptom  of  a  more  general  disease   (bulbar  pnraly*is,  tabM, 

multiple  sclerosis,  etc.). 


r  both  the  adductors  (thyro- 
as  well.  Aphonia,  or  voice  is 
1  part  of.  their  course.    Edges 


May   be    symptoms 
of  central  disease. 


^iiilnier-il  or  bilateral  panlysis  of  the  soft  palaU 
of  nil  the  laryneeal  muscles  and  auestbesla  (t 
larynx. 


Thei 


of  inflammation  of  the  larynx. 


J  History  of  over  use  of  the  voice. 


llyiirrieal  sympio) 


Laryngitis. 
Kxbauallon. 


H>-8t«rIcat  Aphonia.   (748), 


Tremor  and  Ataxia.- 


Tn-miilous  rqi)  slovenly  «peech,  words  are 

badly  formed,  lellem  and  syllables  are  Evidfut 
left  out  both  !d  speaking  and  writing.  '■-'■'L''"oti. 

Scanning  speed). 

Monotonous  speech, 

■Ortntu  letlere  (con 

Ulternnce  Is  arrested  by  a  spa-m  of 


snit. 
lentat   de- 


Spc-ch  i 


I. 


re  are  aphonia  or  boari-uess  niid  nasal  speech  and  some  dysphagia.     There  may  be  respira-     rMay  he  evidence  of  injury  or  of  pressure  upon  pneumogastric  nerve, 
tory  dyspnoea  ond  deglutition   imeumonia.     If  both   nerv.s  are  slightly  affected   there  may 

be  rapid  and  irregular  cardiac  afiion  and  slow  and  irregular  respiroiion  ;  if  severely  affected,    •'  [*ulbar  symptoms  (424)  with  hemiplegia  or  paniplegria  and  exaggerated  tendon  reflci 
death  occurs.  In  pseudobulbar  paralysis  (546.  5531  the  speech  is  also  thick  and  indistinct 

'      In  myastliinia  gravis  (554)    dysarthria  results  from  '-oolinueil  speaking. 
foreign  bodfhas  ia  the  mouth  (hot  potato  speech!  (i-id  fi«iuently  changes  in  pitdi, 
lenomenon   (ft"l-    History  of  syphilis.    Lui 
CbildWini*  and  steadily  progressive  demt 


of  hereditary  ataxia.    In  cerebellar  lesiims.  the  spi'i>oh  i»  o(i>'n  slow,  labored  aud  irregular  and  pbonntion  Is  affected. 

ttacks  mav  ,.^o„;      Oi,il,lld.n«»  and  ^t^-,a\U-  r^r^^l ~ ■     ' a~ '~^f^  puncture  show*  globulin  and  lymphoeyioii..     Patients  are  restless  and  especially  irriiahle  and  violent,  iiHI.ougb  usually  amiable.     .Apoplectiform  aud  epilei.iiform 
tracKs  ma,\  nccui.     (.iiil<]t>Jini)»  ana  sieadUy  progressive  dementia.  Wii'sermann  usually  positive. 

Alcoholic  history.  .I'li'-ir.me:.  trtfor  nod  breath.    Temporary  nature.     r..olii.h  speech  and  actions. 
Intention    Tremor.     Grent  variety  of  widespread  mol«  and  sensory  -ymptoms.     NysUgmus.  e.ta^emted  knee-jerk.  Habinski.    The  speech  is  Jerky  and  -omewhat  resembles  the  scanning  of  ver.e. 

Passive  T«mor.  Rigidity  of  mnsdes  and  slisl.t  fle*n  of  most  joints.    Attit..de  is  tbat  of  bending  fomatd.     Mask-like  face.     Fes tina ting  gait.     Speedi  aUo  shows  fe.tinatlon  at  times.    See  al*.  Encephalitis  Lethargies  (1047). 

spoken  with  difficulty  and  are  repeated  many  times  imperfectly b*re  they  are  finaUy  utUred  explosively.    Speech  U  explosive  and  filll  of  repetition  of  certain  sounds. 

that  words  can  be  uttered.    The  same  is  repeated  several  times  hiT»r«-  .) 


«  .« .h.  „;^  .J."  ioiViVh^n'  ei,',S«?r.",."n«l';nTitM""'  "  "*''"""^"  <«"i'«'«»in-).  Tbm  i.  i:m^,u,  «  „i..i„8  a,  ™.cu  .p.™ 


a  be  spoken.     Thi^  more  the  attention 


Paralysis  of  Pneumognstric  Nerve  trunk,    (7041. 
Bulbar  Paralysis,  {424.  544.  540.  60*.  TW.  IIM)- 


Frledreich's    aud    Marie's    Hereditary    Ataxia,     (10424. 

(VW-l-fift-70-87.  7S2-3).  _    ,„,^    _^, 

Paresis.   (185.  180.  579,  676.  803,  1(W2.  1106.  1216.  1230) 

Alcoholism.    (5K5.    058,    063.    673.    7S1.    ftM.    7031.    tfl.m 

MuS  "ofo'Snated  Sclerosis,    (.-ill,   580,   OT.il.  CC6. 

ftW,  750.  SOS.  ni4.  10541. 
rnmlysis  Agitans.    (Bin.  «,,.  904>. 

Stammering  {Annrthrla   Liternlis).    (720). 
Siultpring    (Anarthria    Si,aimodicft    or  articulalive    tics). 
(729). 


L 


CHART  Xlllb 

Amnesia  and  Aphasia 

Comprising  Numliers  739  on  left  side  of  Chart 
and  772  to  780  on  right  margin 


169 


TEST 


739 

AMNESIA     AND 
(220  to  229). 


APHASIA 


XoiK!  of  these  conditious  con- 
stitiiles  a  disease,  but  is 
ralliiT  one  symptom  of  a  more 
complex  disease.  Each  is  a 
form  of  dementia,  or  more 
accurately,  amnesia  in  the 
l)road  sense  of  the  term  and 
consists  in  a  loss  of  general 
or  special  memories.  See  also 
.\narthria  and  Dysarthria 
(737-8). 

Ill  I'xaininins  patients  for  am- 
nesia or  aphasia,  it  is  most 
iiiipiirtant  to  first  ascertain  to 
what  ilesree.  if  at  all,  they  are 
deaf. 


DIAGNOSTIC   ANAL-: 

AMNESIA.  APHASI 

ABSTRACT    O 

The  loss  of  memory  may  not  be  accompanied  by  any, 
the  names  of  persons  is  rather  common  and  of  no  diaj 
less  distant  past,  are  referred  by  the  memory  to  the  in 
cerebral  concussion  and  compression  (1042-3),  especia 
little  time  immediately  previous  to  the  injury  and  frig! 

Examination  of  the  patient  shows  a  loss  of  memory,  espe 
in  old  people  and  in  the  insane,  and  is  usually  associat 

Patient    is    incapable    of    normal    speech   ..  <-Ian  express  ideas  by  gestures,  but  cannot  name  objects  \J 


Patient   is  capaule  of   normal  speech   but 
exhibits  a  decided  loss  of  memory. 


(s[H)ntaneous,  repeatius  after  dictation, 
reading  aloud)  for  want  of  innervation 
memories  of  a  few  or  many  spoken 
words. 


Patient  is  incapable  of  normal  speech  for 
w.iiit  of  auditoi-y  memories  of  spoken 
words. 

I'atient  is  incapable  of  normal  speech  for 
want  of  \'isual  memories  of  objects. 

I'.itieut  is  incapable  of  normal  speech  for 
want  of  visual  memories  of  written  or 
printed   words. 

Patient  is  incapable  of  normal  speech,  be- 
cause of  a  faulty  co-operation  of  the 
various  cortical  centers  concerned  in 
speech. 


verbs  better  than  nouns  and  proper  names.  IlecogniZi 
tieut  is  frequently  at  a  loss  for  a  word,  llis  vooabular 
phasia — 7TS)  but  is  often  conscious  of  his  mistake  if  h 
matismus),  but  can  often  repeat  sequences  of  numbe 
from  copy,  but  makes  many  mistakes  in  spontaneous  w 
with  right-sided  hemiplegia  in  right-handed  persons  and 

PatieL.  fails  to  understand  more  or  less  of  what  is  said 
what  he  repeats.     Cannot  execute  verbal  commands,  bi; 
conscious  of  tliis  mistake  even  when  his  attention  is  cal 

Patient  cannot  name  objects  seen,  but  may,  at  times,  r^ 
aphasia  has  been  classed  under  the  complex  term  "moti; 

Patient  cannot  read  written  ov  printed  letters  or  words, 
use  a  wrong  word  and,  wiien  they  do  so,  are  conscious, 
many  mistakes  in  spontaneous  writing.     I'atients  cann. 

Patients  suffering  from  this  defect  exhibit  a  combination  i 
groups.  First,  those  in  which  the  symptoms  of  motor  £ 
combination,  incomplete,  of  the  symptoms  of  motor  an 
group  (Transcortical  motor  aphasia)  spontaneous  sp( 
of  the  year,  the  alphabet,  numerals,  etc.)  are  little,  if 
group  (Transcortical  sensory  aphasia)  there  is  more  oi 
(days,  mouths,  etc.,)  are  possible;  although  these  wore 
glee  of  both  sensory  and  motor  aphasia.  Spontaneous 
three  groups  resemble  those  occurring  in  gradual  recov 
impossible  or  defective.  The  patient  omits  words  in  sj 
so  that  the  speech  or  writing,  wueu  po.ssible  at  all.  oft 

Patient  is  incapable  of  spontaneous  writing  for  want  of 
simply  cannot  W'rite.  A  very  rare  condition  uucoi 
left  frontal  convolution  is  iimuediately  above  the  motor 
printed  matter  into  script.     His  copying  is  purely  mecl 

Patient  omits  words  in  writing,  uses  the  wrong  words,  mi 

The  .subject  of  aphasia,  in  its  various  forms  and  subdivisions,  is  a  very  complicated  one  and  is,  as  yet,  far  from  being  solved.    Too  few 

Broca,  in  ISOl.  published  a  case  of  motor  aphasia  with  a  lesion  at  the  base  of  the  left  inferior  frontal  convolution  and  thereby  laid  t 

Wernicke   (vvliose  studies  have  contributed  greatly  to  the  comprehension  of  aphasia)   divided  motor  and  sensory  aphasia  into  three  sub- 

1st.      Cortical  Motor  Aphasia,  in  which  the  patient  is  unable  to  speak,  write  or  read  ahnid  correctly,  or  to  speak  or  write  correctly 

2nd.     Subcortical  Motor  Aphasia,  in  which  the  patient  can  neither  speak  spontaneously  nor  from  dictation  nor  read  aloud  correctly 

3rd.     Transcortical  Motor  Aphasia,  in  which  the  patient  can  neither  speak  nor  write  correctly,  but  CJin  speak  and  write  from  diets 

1st.      Cortical  Sensory  Aphasia,  in  which  the  patient  can  speak  (with  paraphasia)   and  copy,  but  can  neither  write,  nor  speak,  no 

2nd.     Sub-cortical  Sensory  Aphasia,  in  wdiich  the  patient  can  speak  quite  perfectly,  write,  copy,  read  aloud  and  understand  writii 

3rd.     Transcortical  Sensory  Aphasia,  in  which  the  patient  can  speak   (with  parapliasia)   and  write  (with  paragraphia),  can  copy, 

Wernicke  also  recognizes  a  Conduction  Aphasia,  in  which  the  patient  can  speak,  write  and  read  and  undersUind  correctly,  but  exhibit 

Marie  considers  all  forms  of  aphasia  as  resulting  from  a  greater  or  less  degree  of  a  general  intellectual  impairment  i-ather  than  from  lo 
aphasia  wit:h  didiculty  of  arlii'ulalion  (anarthrin  or  dysarthria).  Whether  he  is  altogether  riglil  in  this  or  not.  certainly  our  conccpfir 
nicke's  ideas,  neither  of  which  is  pre  bably  altogether  false.  It  is  to  be  renieml>ered.  however,  that  many  cases  of  dejnentia,  in  all  stages  of 
acteristie.  defects  of  one  or  more  of  the  component  parts  of  the  complex  phenomenon  of  speech.  This  strongly  indicates  a  loss  of  some 
tion  is,  at  the  present  day,  too  firmly  proved  to  be  easily  abandoned. 


.\<;i:apiii\. 


Palicni's  -pecch  is  imninil,  Iiut  his  writing  is  abnormal. 


i   OF   SYMPTOMS 
LND  AGRAPHIA 

lYMPTOMS 

3y  very  little,  iutelloutiuil  imijaii-iuent  iu  other  respects.  To  a  certain  degree  the  loss  of  memory  of 
;ic  or  prognostic  value.  "Retroactive  amnesia"'  is  where  events,  which  occurred  in  the  more  or 
iate  past,  as  in  Korsakoff's  psychosis  (1102).  "Itetrograde  amnesia"  occurs  in  some  cases  of 
iiose  associated   with  fright.     In  it,  memory  is  lost  of  those  events  which  occurred  during  some 


DIAGNOSIS 


.\mnesia. 


y  for  recent  events,  impaired  judgment  and  a 
rith  mental  depresj^ion. 


;eneral  failure  of  mental  powers.     Very  common       Dcinentia    (1079). 


773 


or  at  all.  Patient  knows  the  idea  he  wislies  to  express,  but  cannot  put  it  into  words,  ('an  u.se 
le  desired  woi-d  when  it  is  spoken  to  him  and  can  often  tlieu  pronounce  it.  In  speaking,  the  pa- 
limiti-d  often  to  one  or  two  words,  or  even  to  none  (anarthria — 737).  Uses  a  wrong  word  (para- 
ttentiou  is  called  to  it  and  often  when  it  is  not.  Cannot  construct  sentences  correctly  (agram- 
lays,  months,  etc.,  and  can  sing  songs.  When  his  arm  is  not  paralysed  patient  can  usually  write 
ig  (paragraphia — TSti).  Can  usually  read  but  not  aloud.  The  condition  is  usually  associated 
e-vei-sa. 

im.  Cannot  repeat  what  is  said  to  him,  or  if  in  rare  cases  he  can  do  this,  he  does  not  understand 
adily  executes  wricteu  ones.  In  speaking,  the  patient  frequently  uses  a  wrong  word  and  is  not 
:o  it.    Can  write  spontaneously  and  from  copy  but  not  from  dictation.     He  can  read  well. 


Moi.ir  .Vphasia  or  Aiiheniia  (222,     771 
1402). 


Sensory   Aphasia.      Auditory 
Aphasia.   Word  Deafness 
(222-33,  13S2-82a). 

Visual  or  Optic  Aphasia 
(224.  232,  13.57). 

Alexia.     Word     Blindness 
(220.  13S2a,  1403). 


77(! 


Transcortical     Aphasia.      Mixeii     77S 
Aphasia      (22f)1.      Paraphasia 
(22(1). 


lize  and  name  objects  which  he  touches  and  feels.  His  defect  in  speech  is  not  great.  V'isual 
ihasia,"  of  which  it  may  form  a  not  inconsiderable  part. 

cannot  execute  written  commands,  but  readily  executes  verbal  ones.  In  speaking,  patients  rarely 
lieir  mistakes.  Patient  can  write  from  dictation  imperfectly,  but  not  at  all  from  copy  and  makes 
lad  what  they  have  written. 

otor  (774)  and  sensory  (775-0-7)  aphasia  in  varying  degree  and  can  be  classified  into  three 
sia  predominate.  Second,  those  in  which  the  symptoms  of  sensory  aphasia  predominate.  Third,  a 
nsory  aphasia.  A  sharp  line,  however,  cannot  be  drawn  between  these  three  groups.  In  the  first 
is  disturbed;  buc  repeating  after  dictation  and  reciting  of  serials  (days  of  the  week,  the  months 
.D,  impaired.  Cases  in  tliis  group  run  rather  a  rapid  course  towards  recovery.  In  the  second 
3  fully  developed  sensory  aphasia  and  the  repeating  after  dictation  and  the  reciting  of  serials 
•e  not  understood  when  .spoken  by  themselves  or  others.  In  the  third  group  there  is  some  de- 
ech  is  very  imperfect;  while  the  reciting  of  serials  is  well  preserved.  The  symptoms  in  all 
from  pure  motor  or  sensory  aphasia-  In  all  three  groups  reading  aloud  and  writing  are  either 
ing  or  writing,  or  uses  a  wrong  word  (paraphasia),  or  puts  a  right  word  in  a  wrong  place; 
lecomes  quite  incoherent   (Jargon  speech). 

necessary  innervation  memories.  His  arm  and  luuul  are  nut  paralyzed  for  other  movements.  He 
cated  by  motor  aphasia,  because  the  cortical  area  tor  writing  being  at  the  base  of  the  second 
:ech  center.  A  patient  with  agraphia  may  be  able  to  copy  print  or  script,  but  lie  cannot  copy 
cal.    A  patient  may  be  able  to  write  letters,  sponlauoously.  Ijut  not  words  and  sentences. 

up  words  in  the  sentences  so  that  writing  becomes  incoherent.     He  can,  however,  write. 

les.   scientifically   observed,   have  come   to   autopsy. 

oundation,  not  only  of  the  modern  ideas  about  the  faculty  of  speech,  lint  al.so  of  cerebral  localization. 

sions  each  : 

n  dictation,  or  to  read  with  full  understanding,  but  can  copy  correctly  and  understands  what  is  said  to  him. 

t  can  read,  write  and  undei-stand  what  is  said  to  him. 

1,  can  copy,  can  read  aloud,  and  can  understand  speech  and  writing. 

ipy  from  dictation,  nor  read  aloud  perfwtly.  nor  understand  speech  or  writing. 

lilt  cannot  speak  or  write  from  dictation,  nor  understand  speech. 

e  and  speak  from  dictation,  and  read  aloud  but  all  without  understanding,  and  cannot  undei-stand  either  speech  or  writing 

iraphasia  and  paragraphia. 

•erebral  lesions,  especially  not  to  those  of  the  left  inferior  frontal  convolution.  He  considei's  motor  aphasia  to  be  a  combination  of  sensory 
if  aphasia  previously  to  Marie's  article  had  been  growing  too  schema 'ic.  The  truth  pi-obably  lies  somewhere  between  Marie's  and  Wer- 
■oliipment.  exhibit  no  aphasia.  Furthermore,  cases  of  aphasia  arc  rarijy  permanently  complete  (anarthria),  but  show  varying,  even  ehar- 
nent  of  a  composite  whole  and  each  of  these  elements  may,  in  time,  be  more  certainly  localized.     The  theory  of  a  cerebral  corticil  localize- 


AL-nipliia    (227.   13S!)). 


Paragraphia    ("226). 


770 


7Sl) 


CHART  XIIIc 

Disorders  of  Gait;  Ataxic,  Paralytic  and  Flaccid, 
Paralytic  and  Spastic  Gaits 

Comprising  Numbers  736  to  742  on  left  side  of  Chart 
and  781  to  804  on  ri^ht  margin 

(Note) — -In  addition  to  tlie  diseases  mentioned  in  this  chart,  pain,  whether  in 
the  joints  (rheumatism,  gout,  arthritis,  morbus  coxae,  etc.),  or  in  the  muscles 
(rheumatism  myositis  etc.),  or  in  the  bones  (caries,  etc.),  or  in  the  nerves  (sciatica, 
etc.)  will  cause  a  limping  gait.  The  gait  of  a  patient  suffering  from  weakened 
arches  in  the  feet  is  very  characteristic  in  advanced  cases  and  this  common  disease 
should  always  be  thought  of  in  any  disturbance  of  gait  and  in  any  painful  affection 
of  the  legs  or  lower  back. 


171 


DIAGNOSTIC    SYMPTOMS    AND    TESTS 


DIAGNOSTIC   ANAI 
DISOEDEE 

ABSTRACT    ( 

cli-:onlor  is  (if  a  temporni'y  nature.    Pnlipnt's  sprwh  is  liUuTe<l  and  fooli 


DISORDERS    - 
av  (^AIT. 


740 

Ataxia.     (Incoordi- 
nation   is   the   most 
prominent     s  y  m  p- 
tora.) 
(See   also    7iH).) 


rStaggerina  (lait.      J  Disease  of  permanent  nature.     Patient 

(Keeling  gait.)  sways  from  side  to  side  and  lurelies 

I       like  a  drunken  man.     The  ataxia  is 

j       almost    entirely    limited    to    walking: 

[      and  slandin;;. 


741 

Paralytic  and 
flaceid.      (Weak- 
ness is  the  most 
prominent 
syiii|iti>Hi.) 


742 

Paralytic      and 
spastic    (Stiffness 
is  the  most  prom- 
inent  symptom.) 


'There     Is      a    strong     heredity 
disease  occurs  in  family  groups  ; 
in  youtli.     Nystagmus. 

No  heredity.     Uccui-s  at  any  age. 


IncoonlinatMl   Cait. 
(Stainpiic.;    (iait.) 


Waddling   Gait. 


I'alienI  (lni>s  ncit  \\;ilk  liki'  a   ilninken  man.  but  Uirinvs  his  legs  alxHit  in  ai 
anil  excessive  nianurr.     .\ll  movemeuis  of  logs  are  ataxic.     In  well  markei 
are  raised  li'igh.  Muug  outwards  and  forwards  excessively  and  brought  ba< 
ground  with  hard  st.-inip  on  heel.     The  eyes  are  employe<l  to  control  the 
and  walking  in  lln'  lUirk  is  very  imperfect  or  impossible. 

Mus<-uhir    atriipliy    and    pseudo-hyper-       In   u.ilking  jiaticnt  llirows  body  f 
troidiy.  I       of  others,  but  all  are  weak.      In 

I       seen  at  limes  in  pregnancy  ami 


Muscles  norLual. 


Iligh-steppiuE 
(!ait. 


Feet  drap 
ground. 


Similar  walk.     Congenital.     Usua 
shows  dislocation  of  hip  and  ah 

Cencral  weakness.  es|iecially  of  extensors.     P.ilateral.     .May  be  some  ataxiai 
symptoms. 


Weakness  of  cxteusurs  only,     itilateial.     likie  line  on  gums.     Wrist-drcp  as 
N'arialile  distriluilion.     \\ Cakness,  especially  of  extensors.     Often  unilateral 


In  walkins-  all  uuiscles  of  legs  seem 
too  weak  lo  raise  feet.  No  tremor 
or  spasm.     Steps  short. 


A\ 


ipoiai-y 


.'ibb 
A.lvai 


nrni    c 
■   to   \s:i 


ondiliou    following   il 

■unditiou.   Oi-ganif   an 
:  in   (liis  disease. 

allieromatous  artel 


Hysterical       symp- 


Inability 
on  one  or 


r.oth  legs. 


toms  present, 
lo    stand    ly.-ick  of  will  power 
both  feet,    while        pretending! 

to   have   much. 

Knee-jerk    may    he    One  leg. 

increased.        Faint 

ankle-clonus    often, 

Rabinski     ahvay*, 

absent. 


Tendon  reflexes  in- 
creased. Ankle- 
donus  and  Bab- 
inslci  present 


Toes    .scrape    along 
ground.    T.egs  rigid 
and   frequently 
tremble. 


I'nilateral. 


Legs  can  be  moved  freely  and  no 
parenily  is  afraid  to  walk  or  ha 
(|ueni,   legs  sive  way  under  her 

The  weak  leg  is  drawn  along  aftei 
shows  more  strength  in  leg  than 
moves  badly  in  each  direction    ( 

The  weak  leg  is  usually  swung  foi 
(mowing  gail).  The  leg  is  u.su 
wlmle.  Ill  walking  siih'wsiys  (.-< 
w-arcK  the  Iicallhy  side    (Schiillei 


I'.ilaleral. 


The  legs  are  rigid  and  offer  resist 
so  that,  in  walking,  bcxly  and  slu 
backwai-ds  lo  pull  legs  forwa 
trembling  (clonu.s)  when  bnnu; 
ducted  so  lliat  kiiera  ari'  hehl  1 
in  walking  (scis.sors  gait).  Pe 
of  severe,  anemia  may  be  prescB 


Oeneral   rigidit.y. 


Patient  is  sli;;hlly  bent   foiwards  and  all  his  .ioints  si 
relropulsioii  -  ■!    teuilcnc.v    to  sliigger   b.'ickwaiils.      1 


:S   OF   SYMPTOMS 
3F   GAIT 

SYMPTOMS 

.Markwl  mciit.-il  ilisorder  ami  liistorj   i>f  alculiiilic  ahuso. 

•Occurs  before  puberty.  Knee-jorks  usually  ab^ieni.  i 'niitraoture  and  ilerorruity  nf  fiT-r.  liaKiuski 
\     present. 

Oef-urs  after  puberty  but  in  yiiulb.     Ivufe-jerks  usually  present  aud  exaggerated.     Oculo-uioior 
paralysis  and  optic  atrophy. 

KelraitiiiM  nf  ln-ail.  eerebellar  lits  au<l  Citli.-r  cereliellar  syiuptems  may  be  present. 

,  Knee-jerks    alxilisbed.      .Vrjryll-Uobertson's    pbenomeiioii.    oijtie    atroijliy.      History    of 
rkward  sypliilis  usually.     A  iimiinou  di.sease. 

:es  less      ! 

own  to    J  . 

ements  Knee-.)erks  are  usually  pre.sent.  ilay  be  no  other  symptoms  than  ataxia  and  anes- 
thesia, or  may  be  all  the  spinal  symptoms  of  locomotor  ataxia,  but  none  of  the  cr.i- 
nial.  I'speeially.no  I'ye  symptoms.     A  rare  disease. 

side  to  side  like  a  duck.  Market]  lordosis.  .Vtrophy  of  some  muscles,  apparent  hypertrophy 
nj;  i>atient  pushi's  himself  up  with  his  hands  and  crawls  up  upon  his  own  legs.  (A  similar  gait  is 
ibdomnl  ttimors.) 

rilateral  but  may  be  unilateral.  Xo  change  in  the  muscles.  Hip  joints  unusualy  mobile.  X-ray 
e  of  acetabulum. 

the  walk.     Muscular    weakness,    tenderness    and    atropliy.      Knee-jerks    absent.      Many    sensory 

11  as  foot-drop.      History  of  colic  and  of  exposure  to  lead. 

[liseular  atrophy  williout  tenderness.    Electrical  reaction  of  degenreation.    No  sen.sory  symptoms. 

..     Organic  and  peripheral   relh'xi's  normal.     Xo  sensory  paralysis. 

Tipheral    reflexes  disordered    (lost).  Sensory  paraly.sis.     Patients,  even  with  cniti-hes.  ar.>  rarely 

Loss  of   memory  and   mental   impairment.      Reflexes  normal  or  increa.swl. 

Uy   when   lying   or  sitting.       Patii'Ut   apparently   makes  no   effort   to   w.ilk.      lycgs   collapse.     Ap- 
rg<itten  how  to  walk.     In  otU^'r   cases,    patient   walks    normally:     bul    at    intervals,   usutilly   fre- 
she  falls,  but  never  hurts  herself  seriously. 

!  .strong  mil'  but  never  advances  beyond  it.  In  some  actions,  when  taken  unawares,  the  patient 
aid  be  necessary  for  walking.  In  walldng  sideways  (stepping  laterally  I  along  a  line  patient 
iill  >r"s  side  gait — 450) . 

ds  and  outwards  alwut   the  normal    leg  as   a    pivnt    and     is    set    down    in    advance   i>f    lliis    latter 
strongly   extendiHl  at  the  km-e  and  the  whole  sidi'  of  the  body  is  i-igid  and  swings  forward  as  a 
ling  kitenilly)    along  a  line  the   patient   moves   well    towaiils   the   paralysed    side,    but    badly   to- 
ide  gait      l.">(;). 

Orgiinic  reflexes  are  di.sordered,  and  si'usory  symptoms  are  present, 
N'o  ata.xia. 


Organic  reflexes  may  or  may  not  be  disordered,  sensm-y  symptoms. 
e  to  forw.ird  movements;     I      Marked  ataxia, 
srs  mtisl  often  be  bent  far 


I,egs     freiiueutly    show 
forward.     Thighs  are   ad- 
together  or  even  crossed 
ious,  or  some  other  form 


pVdult. 

Organic  reflexes  not  disordered.  No  sensory  J 
symptoms.     No  ataxia.  1 

'  Youth.  Siassiirs  <i.-iil. 

Dissociation  of  sensation  (80.5). 

Intention   tremor,  marked  ataxia,  at  times  staggering  gait. 


ly  flexed.     Festination  and  propulsion--a  tendency  to  go  forward  at  ever  increa.sing  speed:  also 
ive  tremor.     See  also  Eucephalilis  Lethargica   (1047). 


DIAGNOSIS 

-Vleoholic     Intoxication     ((Jj'S.     tjO,"!.     7S1 

G7:i,  7i:;7). 

Friedreich's    or    Here<litary    Ataxia     7S2 
(0.51,  G70,  GS7,  7(mK 

Marie's    or    Hereilitary,    Cerebellar     "S^! 
-Vtaxia    ((SO,  litiO). 

Lesions  of  Cerebellum  or  its  tracts     784 
((;07-.S-47,  B8-3,  lOlG,  1205). 

1\il>es     {cm,    7.">0,    827,    SiKi.    f)7i),     7R5 
OSS,  1004,  1217,  12S1). 
(Figs.  24-7). 

Ijesions     of     posterior     columns     of     7SG 
spinal   cord    ((VU.   1271.  i:'.G0-?,-4. 
l-itim.       (Figs.    24-G). 

.Muscular  Dystrophies    (477.   Il."i4).     787 


Congenital       Di.slocat.ion       of       the     7SS 
Hip. 

Multiple    Neuritis     (4.SS,    G02.    '<2.">.     7.S9 
lOOS.  1147,  1327). 

Lead    Palsy    (4!I4.   .">S4,    10.",:!).  7!M) 

Aiaite  Anterior   Poliomyelitis  701 

(40."'>,   1148,   12.'?:!).     (Figs.  24-7). 

Weakness   (G71  ) .  702 

Myelitis        or        Myelomalacia       in     VO:! 

lumbar      enlargement       of       ccu'il 

{4.S.J,  S27,  1140,  i:«OL 
Senile   Paraplegia    (.";22).  701 

Astasia     and    .\basia     (2S17.    G,">2).     70." 


Hysterical     Hemijilegia     or     Mono-     70ii 
plegia    (.")27,  1070). 


Organic       Hemiplegia       nv      Mono-     71)7 
plegia.        (Ai)oplexy.     Cerebral     or 
Spinal  Tumor  or  .\bscess). 

M.yelitis      or      Myelomalacia     above     70,'* 
lumbar      enlargement.      including 
Comiiression  Mvelilis 
( .''>i:i-4-7-20-o0,  8.31 ) .     ( Figs.  24-7 ) . 

Ataxic  Paraplegia  700 

(."i2i;.  G(50).     (Figs.  24-7). 

Spastic    Paraplegia     (.">2."i),    incliid-     ,800 
ing  .'Amyotrophic  Lateral 

Sclerosis  (.547), 

Cerebral  Diplegia  801 

(478,  501,  .577,  10.51). 

S.vringomyelia  (5.53,  G93,  840-2,  1000,  802 
11.52,  1170,  1187,  1370-2), 

Disseminated       or         Multiple     803 
Sclero.sis     (oil,     580,     C.59,     G(!(!, 
088.  7.59,  70.8,  914,  1054). 

Paralysis   .Vgitans    (Old,   i;77.   7G0).     804 


CHART  XIV 


Disorders  of  Sensation 


DIAGNOSTIC  ANALYSIS  OF  SYMPTOMS 
DISORDERS  OF  GENERAL  SENSATION  AND  OF  THE  SPECIAL  SENSES 


Symptom 
Analysed 


Alterations  in  Sensation 


r806 
Diminution  of  Sensation. 


807 

Exaggeration  of  Sensation. 


805 

I>isorders  of 
Sensation. 
(See  also 
Perversion 
of  Sensa- 
tion Chart 
XV). 


808 

Disturbances  of  Vision. 


1^811 
Anesthesia  and  Analgesia. 

812 

Dissociation  of  Sensation. 

813 

Loss  of  Muscle  Sense. 


\  See  Chart  XIV  a. 


814 
Numbness. 

815 
Hyperesthesia. 

816 
Perversion. 

817 


•  See  Chart  XIV  b. 


Limitation  of  field  of  vision,  j 


809 

Disturbances  of  Hearing. 


810 

Disturbances  of  Taste  and  .Smell. 


818 

Double  vision  (Diplopia). 

■  819 

Conjugate  Deviation  of 
Eyeballs. 

820 

Pupillary  Abnormalities. 

821 

Ophthalmoscopic  Exami- 
nation. 

822 

Deafness   (anakusia). 

823 

Hyperakusia    (oxyakoia'l    or 
1^      Parakusia. 


•  See  Chart  XIV  c. 


i^  See  Chart  XIV  d. 


■  See  Chart  XIV  e. 


173 


CHART  XlVa 

Disorders  of  Sensation 


Comprising  Numbers  806  to  814  on  left  side  of  Chart 
and  824  to  844  on  right  margin 


V" 


.J 


175 


S06 

DIMINrTIONOP 

CDTANICdllS 

8ENSIBII,ITY 

(130). 


IJIAUNOSTIC    SYMPTOMS    AND    TESTS 


Ml 

ANIOSTHKKTA  usiinlly  com- 
liiiipd  Willi  »onii-  ANAI,CJB8IA 
niirl  THRRMIO  ANIWTllIfl- 
KIA.  nup^i^Inllr  tn  •ovi-ri'  wmpm 
of  the  diiensc  {Si&-50). 
(Vis».  26,  S3). 


'IVudon    ri'llrntfl    diumialicd 
nliM'iil    (Ii-«ioa   of   peripheral, 
leusory  neurons — 472). 


I  (Irk'niiio        relicsea 
inonnnl  (300). 
1  (Pigs.  24-0). 


The  nnMlhexin 
or  Ira  pn>ii<i 


'nrrraponda  lo  llie  distribution  of  n  nerve  or  of  one  of  jl 
H-etl.  in  tiie  distrihiitiou  of  the  nerve  (Figs.  33-38). 


DIAGNOSTIC   ANALYSIS    OF   SYMPTOMS 

ANESTHESIA   AND   ANALGESIA 

ABSTRACT    OK    SYMPTOMS 

.•*.  tli.iii;:!!  iniiiilly  K-ss  r 


In  - 


t)reunio  rellexeB 
■Jisorxleml  (300).  ■ 
{Figs.  3i-7). 


Anc«thMin.  imin  iin<l  miiiwulnr  pnrnlyttis.  tenderness  end  atif'iihy  wi(k-<piisnl  Ji:nl  syniini-'lriciil  in  the  distribution  of  itpiiinl  neivus.     llsunlly  n 
'Oie  onetlirain  oorresponda  to  the  diatrihution  of  a  nerve  root,  hut  Is  less  extensive.    Central  njiuptoms  often  present  (Pigs.  33-38). 

SymptoDis  bllatem).     Acute  »r  ^utiULiitr. 

Sympinms  nuiinly  iinllaternl.  nt  li-u^t  m  6rst. 
iiselc  Benso.      Romberg's   symptom,    Argyll- Robertson    pupil.      Tabetic   eiiii~iis.  RiliinJ 


B  also  a  pnralysiH  of  mniign, 
■y  lit  ii h-oholii;  ulniie. 


.NViii-itLK 


.\&sndn(e<l  with  flacfdd  parnlyeiB.  mii»7iilar  atropliy 
dribhline.    Ineontinenoe  of  IcceA.     Bedsores. 


•pliii-  disturbanceB  in  legs.    Bladder  i^mpty  and 


rOngnnic        reflexes 
I  disordered;   it  may 

he  only  slightly 

(.1001. 

(Fics.  19-30). 


sensory  nouron* — )";{). 


No  motor  pomlysht,  but  marked  ataxia  and  loss  of 
rre<]neri(,     l^lnar  hypi'stheeia  and  pareslhesiae. 

fAasnfiiititl  w-ith  spaslic  paraly&is,  without  niiiECular  iilnipliy.  in  nmis  and  leg^,  or 
Rilstpml   nueathesrin    bounded    ahove  by   a  xonoof  hrp^resthesia. 

ABSoi-lnicd  with  paralysis  of  oraninl  nerves,  ataxia,  symptouw  unilatcml,  nt  least  i; 


royrtssive  eoursc 
-phy 


rSpOiVtic  pnnilyKis  in  both  ann!<  and  leK*.     Priapism 
'  Spastic  pamlysiB  in  Uith  Ir^. 


mduolion  <•(  pain.    Optic  at 
Disturbances  of  rcspii 


early  ^tiiKes,  d>-8arthria  and  dysphngin. 


fo  ml>^•^  pnrnly^a,  nnesclioaia  limited  lo  anal  and  ssenital  re^iion  and  vicinity.  Occuiionalty  dissociation  of  sensation  nceuis. 
poiener.    Reilexex  In  lens  normal. 


Incontini-niv  nf  uri 


Assoaati'd  witli 
or  symptoms. 


Organic  reHexc'S 
usually  norm  III. 
very  rarely  dinor- 
derrf   (300). 


bilateral    mid 


s|int<m  (retraetion  of  neok  and  opisthotonos)  and  I'onviils tons.    Awite  nri*ot  with  fevor.    Kemlie's  sign,     f.umlvir 
■nire  show*  ^luhiiUn  and  increase  of  cellular  elenn'ni*  in  eepeliro-splnal  fluid.    Herpes  facialiB. 


I  Fiyniptoms    ' 

I      pa  vn  lytic. 


f  Aciite  onset. 


lOhronic  onset. 


Moii^i'  pnrnlysi!^  ^v3)icfa  may  be  temporary.    Often  hemianopin.      Usually 
B<n«i-.     Cerebral   symptoms.     Post-liemipleeic  motor  di?»onleni. 

T"'iunllv  motor  imralyais.     Convulsions,  locsl  or  eeneral. 
Inertia    nnd   impairment.     Ohoked   disc  op  optic  in-iirlHs. 


and    toss    of    musel" 
.laeksunian    epilepsy    (5S7,   005).     Menial 


AHfJorinlcl  with 
hysterical  vymp- 
toma  (41f>). 


bntli    of    periphe 
i-cnti-nl  Bcniiory  n 


il     and     of   tlightly 
urons.  (300). 


I   pains.  hyiH'ralgeBla.  dioreir  und  othetnid  movements  and  nta^i'i  in  one 
.  with  •*r'a«tii'  piiralyKis  in  lens.    Bladder 


lliiecid  pavalysiB  and  mnaoulnr  nlrojihy 
I  dribbling.     Constipation,     Pupils  ari'  i 


iii'niit 


hitcrni  half  of  the  body, 
/-Symptoms  bilnli 
'Syniptonii*  nwiinl 


ud  ft 


I  jMii'eslheNiae  in  arms 
SeoliORia  and  kypho)i 


nd  hands  arc  prominent  symptoms, 
i  in  neck  and  upper  dorsid   ri'glon. 


MoMr  wcabnens  and  lr.>nior  of  nnns. 
Spastic  symptoms  In  lees.     Organic 


:  Nei 


DIAGNOSIS 
(1^1,  W2.  !)41.  ll-lin.  I17a.  1321-71. 


.Multiplu  Neurilii.  (4SS,  m'i.  TSO,  1008,  1147,  1327). 

(.eaion  of  I'oitterior  Nerve  Root  or  of  Spiuiil  Se?menl  (laa'i). 

Myelitis  or  Myelomalacia  in  I.iiuibur  Enlnrgrmcut   (485,  "US.  1320), 

Tumor  in  Lumbar  Kiilann-meut   (4S0.  1320). 

Tubes,     Locomotor  Aiairia    ('Htl.  7.'>0.  7.'<5.  MIH.  0711.  '.»W,  1004.  1217. 
1231). 

Myelitis  or  Myelomalacia  In  Upper  Oervical  Resion  (513-1). 

Myelitis  ur  Myelomalacia  in  Dor^l  Ri>^iou  (fll7-5). 

I.esloo  In  Brain  Stem    (535,  iViOl. 

lesion  of  conns  tcmiinalia  of  Spinal  Cord. 

<-eivbml  MeniOiiilU   (.".0,S.  ."00.  (ItlT..   UKW.  IIM.-..   tlHtS-lt.  l^'i*'.)!. 

(Vr.>l.nil   ll.'iii.in-liii^e  i.i-  S..tt.'nlu«:   (.^4,  5S>*.  MIO-I.  HV);{,  limLi;). 

Cerebr.il  Tuaior  {iW7.  fiSO-JS.  TiI9,  .1S7.  M2-n.  (IT,,  *«2,  flOS,  Wll. 

ir>riO). 


■^yinpt.ao!-  iisimlly  unilii(er.il,  .\iie.«tlie'iin  usually  in  form  of  tiemianesChesia.  which  may  be  ti-nnsferri-ii  in  wnie  msii.  Anesthesia  often  diarply  boundei]  by  a 
prominent  anatiiniiciil  bmdmark  (knco,  hip,  dhow,  etc.)  and  not  by  nerve  or  root  dtstributlun.  The  niiesthi-siii  i*  ununlly  unknown  to  the  patient  ami  Li 
discovered  upon  physical  examination,  but  when  discovered  is  usually  more  (.i>mplete  tluin  that  present  in  ctise^  of  organic  diaeuBe.  The  anesthesia  is  not 
rivil.     The  putieut  tan  button  clothes,  write,  etc..  with  anesthetic  hands  without  looking.   No  evidence  of  any  oreanic  di'wise.    Aneslhesin  is  from  Buegcstlon. 


II ,»n-»llu-»ia  Dolorosa   {I,eHii (  Opiic  Thalnaius)    (ia«). 

.Myelitis  or  Myelonuilacin  in  Ceivinil  Kularavuiejit   (VA  laVM. 
r»m..riu  iVrvical  Ki.l,ir=eraent   (T.:.'2.  V.m\. 


Muscular  ati«<pliy,  uiih  flhrilliilinn  of  muNcIes  of  linudii  nml  minx  in  Inl- 
■eflexes  normal.     Very  chronic  «ioi«i*.    Trophic  disturbances  ami  inutllatinu 


ANAfCICSlA  na.1  TIIKRMin 
A\i:sTlTi:SIA  «iih  litlle  or 
n..  TA{rril,E  ANWSTIIKSlA 
(IilSSOCIATin.N  OF  SEN. 
S.VTlON)    ISK.). 


AK1NK8THB8IA. 


R14 
NI'MBNKSR. 


Vmlon  n>ftexes  u!<ually  exna-l 
cen.t.-.l  in  lej-s  (47.1).  OrgnnleJ 
lefli-xe-  little  nr  not  at  all  ■ 
■lisonlered    (itfMll.  ; 


Pnins  (tabelii--1ibc)  and  parcsthesinc  ui  legs  nnd  feet,  Legs  exhibit  a  r 
steadily  increaBlni;  pimlys's.  which  ninv  be  nnllnternl  in  the  early  stages,  ! 
Orsnnii;  reflexes  are  more  or  less  di«onlere<l,     Chronic  or  sub-nciile  course.   "1 


R.'tJexv*  increased.    Spasm  prtvloi 
lull  in  unennal  dei:ree.    Orgnni* 


inatea  over  paral.vsis  in  early  singt-.    nabiDBkl  usually  on  both  f 
(■eflexes  slillhtly  disiftnlered. 


lanolgesia.  HuPmr  lynipim 


..tien   |ile»eiit.  , 


III-. 


uesia  of  the 


Motor  pariilyniij  nnd  hyiien-silheaia  nn  one  side  of  the  limly  nnd  exlri-milieB  :  anal:;) 
I  Muiili  tfiflle  pain  and  sjiinal  epilcpBy  nre  common  symptoms. 


1  Relieves  I'nrly  abolidlied.    Trophic  disliirban< 

side  of  the  fjice  iiTid  ataxia. 

'SllL-iiiii   and  ;i 


i:X.U!.;i-:itATII)N  Ol-  rV'lWSmv^  SKNSIBH.ITY.      llM.e...«tb.^,.  .„,)  l,v,.e,-nlu.«ia  ,.re  ..f  li „ 

meyelilis. 


1   llirmiic  uneslb.-iiiii   ,ind  al   Uw*  also   tactile  ai>-vtlM"<iii  oii  Ibr  ..|.[iM.il.'  .ide   .f  the  bixly  rnol  e\lr.r>iilics. 
till  with  fltnjla  and  anesthesia.     It  ociiiw  hi  mullipli'  neuritis,  tabes,  and  in  I'-sIons  of  posterior  culvimim  of  spinal  cord,  of  bniin  stem,  of  posterior  third  of  iwsterior  limb  of  internal  capsule  and 

■  much  90  thnt  "dioked  tliap"  and  other  symptoms  of  cerebral  liminr  should  be  Boufht  for  in  mich  cnses- 
CTiostie  mine,  ivilli  the  esee|ition  of  the  jipoe  of  hyperealhcsin.  limiting  iihnvc  rhe  iine*ibesin  in  iniuBierwo  ni.v.liiis   or    m.v<b.iiiiilaeiri.      In    smh    ea*es  it   mnken    tbe   iiii|icr   limit   of  tho 


Syria  gamy  elia  or  Centrol  Qliosin  in  Dureal  Region.     (ftSS), 


>*vrinKomyclia  in  I.umhar  I3DlarBi>o<ent.     (Sr^l. 

I  .-.ion  in  lateral  lialt  of  l'on«.     Tbr.indM.«i»  of  r.>*leii..r. 
Cerehrilar  Artery  {1200-1). 

r.i-.iwn-Se(|iiard   PniTilyBia   (MV2.  ."Hi!!,  lisijt.     (|--ii:>..  :;4r.l. 


of  the  parietal  cortex. 

Unilateral  mimbneiw  at  band  nnd  toot.  Meadlly  proCTCHsive.  with  slowly  progrinii 
Biltitenil  nuiubness  ig  of  no  diacnxtttic  importnncr.     It  may  he  either  of  nervJii* 


CHART  XlVb 


Disturbances  of  Vision 


Comprising  Numbers  808,  816,  817  on  left  side  ot  Chart 
and  845  to  871  on  right  margin 
Blindness  may  be  caused  by  a  solitary  lesion  in  the  eye,  or  optic  nerve,  or  optic 
chiasm  Heniianopia  may  be  due  to  a  lesion  of  the  optic  tract,  or  geniculate  bodies, 
or  fasiculus  of  Gratiolet,  or  of  the  carcarine  fissure  region  on  the  median  surface  of 
the  occipital  lobe.  The  cortical  center  of  sight  is  the  cortex  of  the  occipital  lobe. 
The  fibers  of  the  optic  nerve  having  their  origin  in  the  lower  left  quadrant  of  the 
retinal  of  both  eyes  finally  terminate  in  the  lower  margin  of  the  calcarine  fissures  of 
the  left  occipital  lobe  (Fige.  16  and  37),  and  tlie  fibers  from  the  upper  left  quadrant 
of  the  retinal  of  both  eyes  terminate  in  the  upper  margin  of  the  calcarine  fissure  of 
the  left  occipital  lobe ;  and  the  same  relationship  exists  between  the  fibers  from  the 
right  side  of  the  retinal  of  both  eyes  and  the  calcerine  area  of  the  right  occipital  lobe. 
The  central  fibers  of  the  optic  nerve  having  their  origin  from  the  small  area  of  clear 
vision  may  possibly  terminate  in,  or  near,  the  geniculate  bodies,  but  more  probably 
pass  in  the  fasiculus  of  Gratiolet  to  the  occipital  lobe  and  terminate  either  in  the 
floor  of  the  calcerine  fissure  or  more  widely  in  the  occipital  cortex. 


177 


DIAGNOSTIC    SYMPTOMS 


DIAGNOSTIC    AN. 
DISTURBANI 

ABSTRACT    < 

A  yellow  color  of  all  objects  seen  irrespective  of  tlicir  true  color:   xanthopsia    (ye 

A  red  color  (erythropsia)   of  all  objects  seen  irrespective  of  their  true  color  (rerl  v 


I 


SOS 

DISTURBANCES   - 
(IF  VISION. 


PERVRRSION. 


SI  7 

AliSKNCE  OR 

I.IMITATION 

(IK  KIKI.n  OF 

VISION 

(35S  to  3(>2-3). 


A  green  color  of  all  objrcis  seen   irrespective  of  tJK'ir  true  color   (green  vision). 
Muscae   volitaiiti'.s.   twisted   threails  and   irregular  s|)ots  moving  aliout   in   field  of  v 
Flashes  nf  liulit  and  ilark   sim.Is  siirn.unded   by  a   briglit   zone    (glittering  scotoniatji 

Achromatopsia  (;j('>4)  and  lieniicln'omatopsia  occur  in  slight  lesions  of  the  geniculal 

|.llysterical  syniiitoms    (41.'"))    are  presei 
.Vn   inversion    (red  having  a   larger  field 

than   the  blue — 14)    and  an   interlacing    T  flioked  <lisc  and  other  symptoms  of  bi 
of  the  color  fields   (Dyschroniatopsia) .       I      creased   iiitra-i  lanial   pressure  is   rel 


f  Peripheral  cause. 


BLINDNKSS 

(358,   1334).    . 


•  '■■nlral  i:iu>e. 


fOcidar  lesions,   such   as  cataract,  optii 
(Jninine.  in   t'lyic  doses,   may  cause  inl 
dilnlalinn   td'   tlic   pupil.     In   either 

Ilil.iteral.        Nr   lesinti    in    eye.      Pupillary    reflexes 

r  No  lesicin   in   eye.     Optic  neuribis  ma; 

Unilateral   1  Nfp  Irsimi   in   rye.     No  optic  neuritis. 
I      max    be  slu>\vn   Hint  the  blindness  is 


Xii    hemiiiiiir    |)n|)illary   rellrx.      No   he 

Homonymous    Tcl.arlanopi.a    ov   (.Quadrant  cir  oilier  paralysis.     May   or  may  n( 

1  lemiamiiMa.  disc.     Very  rarely  occmrs  in  lesions  ( 

i>r  optic  fasciculus  of  opposite  side. 


'No   lii'iiil.-ini'sllii'sia.        Nn   heniiopic  pu] 
(2(!).    No  uili 

Homonymous  heininnopi.T  (14.  3(i2, 
1:137)  may  very  rarely  be  bilateral, 
due  I.I  doiilib'   lesion. 

Ileniiaiiesthesin. 


May  or  may  not  be  a  hemiplegia. 
[)ui)illar.v  reMe.v.  Paralysis  of  moi 
abducens  nerve  or  butli. 


Bitemporal  hemianopia    (3(i2,  1.3.3.")).  r 

j  Slow  onset,  progressive  coi;rse,  tcrmina 
in  complete  blindness.  Clioke<]  disc, 
pupi]|;ii\v  iM'fiex. 

Occurs  in   lesions  of  tJie  retina,  or  of 

IMiesc  may  occur  as   (lie   result  of  sma 
neig'liborhoo<l  of  the  calcarine  fissure 

'  Increase<l  tension  of  cveball.     Rxcavai 

Cupf 

No    incr<>ased    tension    of  On    opi 

eyeball. 

Il.vsterical   symiitiinis    (41."))    are   prese 

.Symptoms   of  l.'ilics   are   present,   especi 
or  no  alaxia.      History  of  Syphilis. 


Nasal  li.inian.ipin    (302,  13.30). 

Horizontal   hernia nopin. 
llninonymous  scotomnta. 


Concentric    limitation    of    field    of    vision. 
even  to  complete  blindness. 


{SIS    OF   SYMPTOMS 
i   OF   VISION 

SYMPTOMS 
I  vision ) . 

I'). 


I.     Sci'ii  rs.|icciiill.v  when  eyi's  aro  (iiriipil  towanls  a  bi-ij;lit  lislit. 


iiiMiiily  .ippoariiii;'  iiud  clisippearini;  in   tlic  field  of  visimi. 


iilii's.  ,il'  tlio  optic  fii^ciciiliis  and  especially  of  llie  calcariiic  riortex. 


disease  are  present.     The  color  field  becomes  normal  after  the  in- 
d.     (Cushins.) 

uritis,  retinitis.  srlaciCTmia.  etc.,  may  cause  blindness. 

?  spasm   of   the   retinal    arteries.      Belladonna    may   cause   extreme 
blindness,  or  semi-blindness,  may  resnlt. 

mal.      Uri'mic  aniiiiirosis  may  be  in  this  class   (edema). 

present.     I'upiUary  reflexes  absent. 

pillary  ri  tlexes   normal.    Hysterical   symptoms.    By  tests    (12)    it 
real. 


DIAGNOSIS 

Jaundice,    or    Santonin.    Amyl     Nitrite.    Cannabis     S45 
Indica  or  Picric  Acid  Poisoning. 

Xeiirasthenia,  Hysteria,  great  emotional  excitement     S4() 
and  after  cataract  operations;  also  after  the  eye 
has  been  exposed  for  a  long  time  to  an  electric  or 
oUier  bright  light    (snownblindness). 

Diseases  of  optic  nerve  and   retina  and  after  eata-     S47 
ract  operations. 

N(Mirastheuia,  circulatoi-y  distnrban<'es  in   brain  and     848 
digestive  disturbances. 

Migraine    and    Aura    of    Epilepsy    and    circulatory     849 
disturbances  in  brain   (575,  S.5S.  1028-61). 

Acliromatopsia  (364).  850 

Hysteria  (lOTfi).  851 

Cerebral  Tumor   (830).  852 

Ocular  lesions.  852a 

Drugs.  S52b 

Lesion  or  edema  of  both  occipital  lobes.  853 

Cesion  of  optic  nerve  or  cliiasni    (^!I4).  854 

Hysterical  .Vniblyopia.  855 


nesthesia    rl^pper  homonymous  cpiadraiit  of  ear-h   fielil   of  vision. 

p  choked    -' 

>tic  tract     I  Lower  homonynnms  (juadvani   of  each   field   of  vision. 


T.esion  of  lower  lip  of  contralateral  calcarin"  fissure.     856 
r.esion  of  upper  lip  of  contralateral  calcarine  fissure.    857 


|- Sudden    onset    and    of    short    duration.      Often    more 

marked  in,  or  limited  to,  one  eye.     No  other  s.vmp- 

I      toms  except  nervousness.     Oireiilntory  disturbances. 

ry  reflex    -|  Clinked  disc.     Slow   onset.     Pivigressive  course  of   tlie 
aralysis.     ;      disease. 

I  No  clmked  disc.     Rapid  onset.     Pennanent,  not  pro- 
t     gressive,  or  rarely  shows  a  regressive  course. 

.\o   hemiopic  pupillary   n-IIex.      .N'o   choked   disc.      Re- 
gressive coui"se. 


Aura  of  migraine. 


858 


lemiopic 
oculi    or 


usually 

lemiopic 


iChoki'd  disc.     Slow  onset.     Progressive 


No   choked   disc.     Rapid   onset.      S.vmptoms   of  menin- 
gitis may  be  present. 

^r.ilal,.ral. 


T'nilateral. 


Tumor    involving    median    surface    of    contralateral     K'lll 
occipital  lobe  cjr  fasciculus  c]f  (Jraliolel    (i:{78). 

Hemorrhage  or  softening  in  or  near  contralateral  c-;il-   8611 
canine  fissure  or  optic  fasciculus  of  Gratiolet   (1378). 

Hemorrhage  or  softening   in   the  posterior  part   of     SiCI 
posterior  limb  of  confalateral  internal  capsule. 

Tumor  involving  contralateral  optic  tract  or  genie-     802 
ulate  bodies   (S9o,  1337). 

NcHiritis  or  lesion  of  contralateral  optic  tract   (895,     St!,'? 
1337) 

Tumor    compressing    central    part    of    optic    chiasm     801 
(894,  13.35).      (Enlarge<i  pituitary). 

Tumor  compressing  homolateral  outer  part   of  optic     805 
chiasm   (894,  1336). 


c  nerve  or  obiasni,  invloving  their  upper  or  lower  portion. 

sions  in  the   geniculate   bodies,   in    the   optic   fasciculus   lu-   in    the 


Horizontal    hemianopia. 
Homonymous   scotomata 


866 

807 


and    final    atrophy  of   optic   nerve.      Pupils   dilat>il    and   unequal, 
of  disc. 

moscopic  I'xamiuation  the  optic  papilla  shows  atrophy. 


Glaucoma    (944). 


Optic  .itrophy   (S9S). 


Pfl8 


80!) 


H.vsleria    (1070). 

Argyll-Rorbertson   phenomenon   an<l   absence  of   knee-jerk.    Little        Tabes    (001). 
)bulin  and   lymidmcytosis  in   cerebro-spinal   fluid. 


870 
871 


808 

D 

I 
S 
T 
U 
R 
B 
A 
N 
0 
B 
S 

O 

F 

V 
I 
S 
I 

o 

N 


O 
o 
n 
t 
1 
n 
a 
e 
d 


CHART  XIV  c— Disturbances  of  Vision 


DIAGNOSTIC   ANALYSIS   OF   SYMPTOMS 


Chabaoteb  of  thc 
Diplopia 


Secondaby  Displacb- 

Deviation  ment  of 

of  Sound  Visual 

Ete  (29)  Axis  (28) 


fB 
I 
N 
O 
C 

u 

L 
A 

R 


818 

Double 
vision. 
Diplo- 
pia 

(383-4). 
(Fig.  18) 
(Displace- 
ment of 
visual 
axis) 


The 
images 
separate 
and  oome 
together 
again 
when 
the  eye- 
balls are 
turned 
from  one 
side  to 
the 

other,  or 
upward 
or 

down- 
ward 
and  back 
again. 


Inward. 


Inward. 

Strabismus 

convergens. 


Outward.    Outward. 

Strabismus 
divergens. 


Limita- 
tion 
of 
Motion 

Outward. 


Inward 


Position 
OF  False 

lUAOG 

(See  28) 


Graphic  Represen- 
tation OF  the 
Diplopia. 
Broken  Line  is 
THE   False   Image. 


On  the  same 
side  as  the 
affected  eye. 

On  the  op- 
posite side 
to  the  af- 
fected eye. 


u 


ii 


Upward. 


Downward. 
Strabismus 
deorsum  ver- 
gens,  slightly 
divergens. 


Upward 

and 

somewhat    side    to    the 


Above      and 
on     opposite 


inward. 


affected  eye, 
image  tilted 
top    inward. 


ii 


di 


i 


Etown- 
ward. 


I  Down 

I  ward 
and 
I  inward. 


Upward 

and 

inward. 


Upward.  Stra- 
bismus sursum 
vergens,  slightly 
divergens. 


None  or  slightly 
upward  and   in- 
ward.    Strabis- 
■  mus  sursum 

vergens,  slightly 
convergens. 

None  or  slightly 
downward  and 
inward.  Stra- 
bismus deorsum 
vergens,  slightly 
convergens. 


Down-  Below      and 

ward  and     on     opposite 
somewhat     side    to    the 
inward.         affected   eye. 
image    tilted 
top  outward. 

Rotation      Below      and 
down-  on  same  side 

ward  and      as     the     af- 
somewhat     fected      eye, 
outward.      image    tilted 
top   inward. 


i      I 


4 

u 

t 

t 

» 

- 

% 

% 

p 

A 
R 
A 

L 
T 

S 

T 
S 

o 

V 


Diagnosis 


r  Ex-    872 
temal 
Rectos. 

In-     873 

temal 

Rectus. 


Su-     874 

perior 

Rectos. 


Rotation 

upward 

and 

somewhat 

outward. 


Above  and 
on  same  side 
as  the  af- 
fected eye, 
image  tilted 
top  outward. 


\ 
« 

i 

R 

I 

The 
images 
do  not 
separate 
and  come 
together 
again  as 
eyeballs 
are  turned 


.\bsent.  May  be  variable.  The  limitation  of  motion  and  the  position 
of  the  false  image  are  the  reverse  of  those 
in  paralysis.  There  may  be  present  some 
irritation,  especially  in  the  nose  or  teeth, 
which  would  cause  a  reflex  spasm.  The 
spasm  is  usually  more  transient  than  a 
paralysis.  The  muscles  usually  affected 
are  the  internal  rectus  and  the  inferior 
oblique. 


In-      875 
1  ferior 
Rectus. 


Su-     876 
perior 
Ob- 
lique. 


In-     877 
ferior 
Ob- 
lique. 


Spasm  of  the    878 
ocular  muscles. 


The  whole  eyeball  can  be  seen  to  be  displaced. 


MONOO 
ULAR 


No  changes  visible  in  eye. 


Hysterical  symptoms  (415)  are  present. 


Two  openings  can  be  seen  in  pupil. 


Changes  visible  in  eye. 


Displacement     879 
of  eyeball. 

Hysterical  880 

diplopia. 

Double    pupil-   881 
lary  opening. 


By  oblique  illumination   the  lens  can  be   Cataract 
seen  to  be  opaque  in  patches. 


882 


Examination    shows   dislocation    of   lens.  Dislocation   of  883 

or  detachment,  or  tumor,  of  the  retina.  lens  or  retina. 

Examination  shows   astigmatism  and   an  Irregularities     884 

-irregular  contour  of  the  cornea.  of  cornea. 


819 

Conjugate 
deviation 
of  eye- 
balls. 


("Associated  w4th  other  symptoms  of  lesions  in  the  pons.  Eyes 
turned  away  from  the  side  of  the  lesion.  Deviation  is  usually 
not  present  when  the  eyeballs  are  at  rest.  A  vertical  devia- 
tion of  the  eyeballs  occurs  very  rarely.  It  is  associated  with 
a  lesion  of  the  corpora  quadrigemina.     (1294.) 


.\asociated  with 
other  symptoms  of 
lesions  of  the  brain 
above  the  pons. 


Eyes  turned  to  the  side  of  the  lesion. 


Eyes   turned   away  from   the  side  of  the 
lesion. 

179 


Lesion  near  the  anterior  por-  8^ 
tion     of     the     pons,     cephalad 
to    the    abducens    nucleus,    in- 
volving   posterior    longitudinal 
bundle. 

Paralytic  lesion  in  almost  any  886 
part    of    brain,    especially,   in 
posterior  part  of  frontal  lobe. 

Irritative    lesion    in    cerebral  887 
cortex. 


CHART  XlVd 

Abnormalities  of  Pupil  and  Optic  Papilla 

Comprising  Numbers  820  to  821  and  890  to  893  on  left  side  of  Chart 
and  894  to  915  on  right  margin 


181 


DIAGNOSTIC    SYMPTOMS    AND    TESTS 


■DisordeivJ  i)ni)ill.iry  reflL'x  to  light  aud  accommodatiou   (330-1). 
Mydriusis,  miosis  i>r  uueqiial  ijupils   (339-41). 


AliXORMALITY 
OF  I'UI'IL. 


S90 

The  hemiopic 
pupilliiry  re- 
flex    (■?).    (30). 


S91 

The  Argyll- 

RolltMiSOIl 
,  phi'linllirlioll    t-l;l7 


Bitemporal  homianopia  (362,  1335). 

1  liii.iciiymcus  ln'iniauopia    (•W'2.   13;'.7i. 


Histoi-y  of  syphilis.      I.yiiiiilnnyli.sis 
in   (■iTt'biM-spinal   Uuid. 
I'lisitivi'   VVasscrmann. 


Tii'linitis. 


No  markpd  symp- 
toms of  cerebral 
disoase. 


DIAGNOSTIC    ANAL' 

PUPILLARY    ABNORMALITIES    ANI 

ABSTRACT    () 

These  phenomena  occur  in  too  mauj 
Their  significance  has  been  discussi 

Choked  disc.     Symptoms  progressive, 


Often  hemiplegia  or  paralysis  of  era 
history  of  syphilis.     Very   rarely  ii 

(Ataxia.  Absence  of  knee-jerk.  Light 
Mental  impairment.  Blurred  speech. 
Rarely  occurs.  Xo  ataxia.  Knee-jerks 
Albumeai  and  casts  in  urine. 

Sugar  in  urine  and  in  blood. 

Lead  in  urine. 


Examination   of  the  blood  shows  a 
condition  of  severe  anemia. 

Urine  and  blood  normal. 


821 

ABNORMALITY 
OP  PAPILLA. 

Disfovered  by 

Ophthalmoscopic 

Examination. 


S02 

0|>tif   neuritis. 

Clioked   disc. 


893 

Opiie  .-ilvopliy. 


Bilateral. 


No    retinitis. 


Marked    cerebral 
symptoms,     espec- 
ially headacie. 


Well  marked  history  of  traumatism  ii 
paral.vsis. 

Increased  size  of  head  and  fontanelle 
be  increased  in  size,  the  pressure 

Retraction    of   head.      Cerebro-spinal 


General  convnlsiou  or  Jacksonian  epi 
lepsy  is  common.  May  be  loca 
paralysis.  Reflexes  usually  in 
creased. 


Cenliellar.  but   no  motor  ataxia.     Ce 
Unilateral.       Local  inllnMiiiinli(iii  can  usually  bt  discovered  by  examining  the  e.ve  and  or 
("Secondary. 


Bilateral. 


Unilateral. 


It  may  be  the  terminal  stage  of  a  neuritis  and  hence  f 
Traces  of  the  active  inflammation   (old  hemorrhages  : 

Old  age.  Usually  atheromatous  arteries  and  high  arte 
Loss  of  knee-jerk.  Miosis.  Lightning  pains.  Bladder 
UneqimI  pupils.  Impairment  of  speech.  Tremor.  Men 
( Characteristic  tremor  or  other  s.ymptoms  of  this  di.seasc 
Local  indniuuinliim  or  lesion  can  usually  be  discovered  on  careful  examinati 


Primary.  No  signs 
of  a  former  in- 
flammation. 


OF   SYMPTOMS 

'TIC    NEURITIS    AND    ATROPHY 

lYMPTOMS 

itions  to  be  of  umcli  diagnostic  importauce. 
Chart  Vb. 

ninating  in  blindness.     Often  associated  with  acromegaly. 


Tumor   compressing 
1335-G). 


DIAGNOSIS 


ihe   optic   cliiasm    (So-i.   S(>4-">, 


nerves.     Optic  neuritis  or  symptoms  of  meningitis.     At  times  a 
ant  hemianopia  in  partial  lesions  of  the  geniculate  bodies. 

pains.     GirJle  sensation  and  tabetic  cuirass. 

raxia.    Restlessness.     Childishness.     Uncontrollable. 

sent.   May  be  no  mental  impairment.     Normal  speech.   No  apraxia. 

Headaches,  especially  in  morning.     Usually  edema  o£  some  part  of      Brlght's  Disease, 
body.     Dyspnoea  on  exertion  and  loss  of  strength. 


Lesion    of    coutoalateral    optic    tract    or    geniculate 
bodies    (W)2-3,  1337). 


Tabes   (611,  829,  912). 
Paresis   (913,  llOfi). 
Syphilis  (1205). 


(Kgs.  24-7). 


Great   thiret  and      Diabetes   llellitus    (1174). 


['rogressive  emaciation    and    loss    of    strength, 
polyuria.     Large  appetite.     Dry  skin. 

Blue  line  on  gums.     History  of  lead  colic.     Wrist-drop.     History       Lead    Poisuiiing    (4'.i4. 
of  exposure  to  lead  poison.  10.")o). 

Dyspnoea  on   exertion   and   progressive  weakness.      Pallor  of  skin      Anemia  or  LouUimia. 
and  mucous  membranes. 


7<;,    TiSl,    71(;.    7!M).    989, 


History  of  syphilis.     Argyll-Robertson  pupillary   reflex.     LymphO' 
cytosis  in  cerebro-spinal  fluid.    Positive  Wassermann. 


Syphilis  (1205). 
ich  the  nerve   has  been  injured.    Usually  complicated   with   facial       Injury. 


894 

895 

896 
897 
898 
899 

900 

901 

902 

903 

9(H 


d  sutures  open  in  the  young.    In  adults,  in  whom  the  skull  cannot       Ilydrocppbnlns   (901). 
reater  and  tlie  optic  neuritis  and  headache  are  more  intense. 


nphocytosia.      Fever. 

May  or  may  not  be  fever.  At  times  a  latent  period.  Primary 
supp\iratiou  of  bones  of  skull  or  elsewhere.  Optic  neuritis  pres- 
ent in  abimt  53%  of  cases. 

No  fever.  Usually  steady  progression.  Optic  neuritis  present  in 
about  80%  of  all  cases ;  almost  invariably  present  in  tumors  in 
the  posterior  fossa  and  in  those  associated  with  internal  hydro- 
cephalus. Tumors  in  pituitary  gland,  corpus  callosum  and  in 
the  central  convolutions,  especially  extra-cerebral  tumore,  often 
show  no  optic  neuritis. 

;llar  fits. 


Meningitis    (.-*0.  005). 

Cerebral    .Misress   or   Sinus   TbrrnnUosis    (.508). 


<^M■^llr;l]   T'lmmr    f."07. 


7S). 


Cerebellai-  Tumor  or  Abscess 
(fi07-S-53-S0,  784.  1016,  1295). 


905 

906 
907 

90S 


909 


iw  any  of  the  causes  of  neuritis  mentioned  above, 
exudates,  etc.)  can  usually  be  seen. 

ten-iion. 
iturbance. 

impairment.    Restlessness.    Unreasonsbleness.    OhiUlisihi'.ess. 
n  usually  be  discovered  on  careful  examination. 


Terminal  stage  of  Optic  Neuritis    (S09). 

Senile  Optic  .\tropby. 
Tabes   (829).     (Figs.  24-7). 

Paresis   (1100). 

Disseminated   Sclerosis    (000). 

Disease  of  the  eyeball  or  orbit   (IS-SS). 


910 

911 
912 

913 

914 
915 


CHART  XlVe 

Abnormalities  of  Hearing,  Taste,  and  Smell 


DIAGNOSTIC  ANALYSIS  OF  SYMPTOMS 


Diagnostic  Symptoms  and  Tests 


809 

D 
I 
S 
0 
R 
D 
E 
R 
S 

0  ' 

F 

H 
E 
A 
R 
I 
N 
G 


822 
D 

E 
A 
P 
N 
E 
S 
S 


A 
N 
A 
K 
U 
S 
I 
A 
(355) 


I. 


Usually 
unilat- 
eral. 
May  be 
bilat- 
eral. A 
perma- 
nent 
symp- 
tom. 


Bone 

tion'  f^"^ 
im-  P^.*"^- 
paired.y^'^- 


Abstract  of  Symptoms 

'Severe    paroxysmal    vertigo  and 
I  tinnitus  aurium. 


I  No  vertigo.       May   be  heredity. 

Locomotor     ataxia     or    dissemi- 

l,nated    sclerosis   may   be  present. 


Diagnosis 

Meniere's  or  918 

Labyrinth  disease 
(649,  685,  1019). 

Atrophy  of  aud-    919 
itory  nerve. 


Bone    May  be  i  May     be     history     of     syploilis, 
con-      asso-        |  symptoms    of    meningitis,  symjj- 

toms    of    tumor    at    base,    optic 

neuritis,  etc. 


due- 
tion 
not 


ciated 
with 
facial 
im-  paral- 
paired.  ysis. 


Tumor  or  inflam- 
mation involving 
auditory  nerve 
trunk. 


I  Disease  of,  or  injury  to,  middle  Lesion  of  ear. 
i^or  outer  ear;  cerumen- 


920 


921 


Usually 
bilateral. 
Very  rarely 
unilateral, 
and  then 
only  a 
transitory 
symptom. 


r  Associated  with  symptoms  of  lesion  of  the 
I       fKjns  or  crura  cerebri. 


Associated  with  symptoms  of  lesion  of  the 
cerebral  cortex.  Complete  deafness  does 
not  always  occur  in  a  bilateral  lesion  of 
the  temporal  cortex. 


Bilateral   lesion      922 
of  the  lemniscus. 
(Fig.  20). 


Hysterical  symptoms  (415).     No  symptoms 
of  organic  disease. 


Lesion  of  the 
temporal  cortex 
on  both  sides. 
(Fig.   15). 

Hysterical  deaf- 
ness (1076). 


Deafness   may   be   caused   by   lesions   in  the  ear  or 
auditory  nerve  or  by  bilateral  lesions  in  the  brain 
stem.     There  is  reason  to  believe  that  the  cortical 
center  (or  area)  for  hearing  is  in  the  anterior 
transverse    tecporal    convolution  which  is  situ- 
ated  in    the   percular  (upper)  surfaec  of  the 
superior  temporal.     Innervation  may  bilateral. 

WORDS  ONLY.  Sensory  aphasia  (223)  is  present. 


923 


924 


924a 


823 

HYPERA- 

KUSIA, 

OXYAKOIA 

OR  PARA- 

KUSIA 

(372,  389). 


810 

DISORDERS 
OF  SMELL 
AND  TASTE 


f  Hysterical  symptoms  are  present. 

Inflammatory  lesions  of  ear  or  its  neighborhood  are 
present. 

Facial  paralysis  is  present.  Low  notes  are  especially 
painful.     Tinnitus  aurium  is  present. 

Very  little,  if  any,  diagnostic  significance  can  be  attached 
to  disturbances  of  smell  and  taste.  The  cortical  area 
for  .smell  seems  to  be  in  the  comu  Ammonis;  while 
that  for  taste  is  probably  slightly  posterior  and  ex- 
ternal to  the  olfactory  area;  but  no  case  has  been  re- 
corded where  loss  of  taste  or  smell  has  been  proved 
to  be  due  to  anv  cortical  lesion. 


Lesion  of 
transverse 
temporal  convolution 


Lesion  of  left        925 
superior  temporal 
convolution. 
(Fig.  15). 

Hysteria  (1076).  926 

Hyperemia  of         927 
inner  ear. 

Facial  paralvsis      928 
(1333). 


181 


CHART  XV 


Perversion  of  Sensation:  Pain  and  Vertigo 


DIAGNOSTIC  ANALYSIS  OF  SYMPTOMS 


DISORDERS  OF  SENSATION— PERVERSION 


Symptoms  Analysed 


r931 
PAIN 
(374). 


930 

PERVERSION 

OF 
SENSATION 
IN  NERVOUS 
DISEASES 
(347). 


Location  of  Pain 

r933 

PAIN  IN  NERVE 

Pain  limited  to  the  trunk  and  branches  of  one 
nerve  in  any  part  of  the  body,  except  that  at 
the  height  of  the  attack,  there  may  be  a  mild 
radiation  of  the  pain  into  corresponding  nerve 
of  opposite  side  or  into  adjacent  nerves. 

934 

PAIN  IN  HEAD.  HEADACHES  IN 
NERVOUS  DISEASE 

After  a  careful  examination  with  suitable  instru- 
ments has  proved  the  absence  of  glaucoma, 
jiritis,  muscular  insufficiencies  and  i  other 
diseases  of  the  eye,  of  the  nose  and  its  sinuses, 
of  the  teeth,  of  the  ear,  of  the  scalp  (rheuma- 
tism) or  of  the  crjmial  bones  (periostitis, 
caries). 

935 

PAIN  IN  TRUNK  IN  NERVOUS  DISEASE 
After  a  careful  examination  has  proved  the  ab- 
sence of  Pott's  disease,  rheumatism  of  spine  or 
trunk  muscles,  arthritis,  disease  of  breast,  peri- 
carditis, pleurisy,  aneurism,  pleurodynia,  peri- 
ostitis, cancer  and  other  tumors,  colic  (intes- 
tinal, uterine,  biliary,  renal)  dyspepsia,  pan- 
creatitis, appendicitis,  peritonitis,  gastric  ulcer, 
gastritis,  enteritis,  hernia,  floating  kidney, 
tubal  pregnancy,  pelvic  inflammation,  intestinal 
obstruction,  etc. 

936 

PAIN  IN  EXTREMITIES  IN  NERVOUS 
DISEASE 

After  a  careful  examination  has  proved  the  ab- 
sence of  any  disease  of  the  bones,  muscles, 
joints,  blood  vessels  or  skin  of  the  arms  and 
legs.    Flat  foot  must  Iw  excluded. 


See  Chart  XV  a. 


932 

VERTIGO 
L(392). 


See  Chart  XV  b. 


See  Chart  XV  c. 


See  Chart  XV  d. 


185 


CHART  XVa 

Pain  in  Nerve,  Pain  in  the  Head,  Headache 


Comprising  Numbers  933  to  934  on  the  left  side  of  margin 
and  937  to  968  on  the  right  margin 


187 


DIAGNOSTIC    SYMPTOMS    AND    TESTS 


DIAGNOSTIC  ANAITSIS   OF  SYMPTOMS 
ABSTRACT    OF    SYMPTOMS 


Tl. 


iJjiTrnnlml  diamnsie  be- 
incoii  ni'iirilis  aiul  upuralgriii 
I'flDnut  nitvays  be  mnile  clio- 
)call7.  l%e  itiapiMis  is  Mf\ 
by  the  experience  Ihat  certain 
oervM.  such  s«  llie  sdatic. 
neuritis; 
(  the  Ul- 
lore  prone  to 
I.  33.  3St. 


A  history  uf 
herrfilj'  or  other  evi- 
dence of  n  neuro- 
palhic  preriiniioaitioD. 
ronton  iliil  nr  nc- 
iIuIrMl.  iB  ciimoion. 
Pflin  \s  unilnlcral  and 
is  iDcri'ANvl  bj  move- 
ment tind  by  eipo- 
Mirc  to  colli  or  wind 
nnil  [a  S'lmctimes 
niwnciDled  nilti  mus- 
di'  ■rpRnm.  Vmi- 
mnior  nml  irapbic 
dUriirliiini'i"<  nrv  ofteo 
prpwnt 


Poin.     uoctumal. 
Moall      area      ai 
•pressing. 

Pnin  loalixcd  in 


l<]vii1eiio;  at 
polMODlng. 


SIny  ill-  i'omt  vnso-motnr  '""  "o  tropliitr  ilistiirbnncc.  excppt  rnrely  a  bIow  blancbing 
ot  tlic  hail.    Ne?er  Jiny  oliH-lricnl  reaction  of  deecncration.     Patient  naually  anemie 


Certain  points  on  Hip  ncrie  are  usuollj  tender  Vpoinls  of  Valletx).     Freqiii-ntly  the  parts  supplied  by  Hie  nerve  are  hyperestlietie      Neimilgia    (llfi.  ]71l. 
ami  local  spasms  occur.    The  neuralgia  may  be  only  one  aymplora  ot  a  more  gcaenil  duiease  (aymptomatic  neuralgia)  or  tndepeod- 
ent  ot  any  oth'ir  rtisrnse    (idiopntbie  neuralcia). 


ConlimiouR  pain   i 
eiacerbatioDB. 


Pain  limited  t«  the 
whole  or  a  portion  of 
Che  trunb  and  dia- 
trihutioa  of  the  trige- 
minal (prosopalgia)  or 
occipital  nerves.  Dl»- 
cases  ot  the  eye,  the 
nose  and  Its  sinnae*, 
the  teetli,  the  ear,  the 
scalp  and  tbc  bonea 
must  first  be  excluded. 
(For  the  dlagnosia 
bctn'eea  neuritis  and 
neuralgia  see  933). 

Pain  strictly  limited 
to  one  lateral  halt  of 
the  head. 


Pain   as   if   atU    -were   bdi 

driven  tbroiifli  the  skull. 

History  or  other  evi-      Pair 
dencc  of  Bjrpbilis  (not 
always  obtainable). 


May  be  boll  vnso-motor  and   trophic  j  tender! 
disturbanO'a  and  there  may  also  be  i 
the  electifcal   reaction   ot  degenera-i 
lioo.     Geieral  health   usually  good.    Nerve  whi 


!A  tumor  may  Ix;  felt  or  rarely  seen  witJt  X-ray  on  nerve, 
A  tumor  or  n  displaced  Iwnc  or  other  Bubataiices  may  be  felt  or  aeon  with  X-ray  oear.  and  corapressii 
liash  or  herpes  lin)itf<I  to  distribution  ot  nerve.    Lymphocj  tosis  in  the  cerebro-spinal  fluid. 
t     seusory  or  motur  paralysis  is  present  in  tie  later  stages.     The  disease  is  caused  liy  inlTai 

to  and  involving  the  n 


in  llie  early  stages  ot  ibc  disease.     Occasi"nnlly.  but  rarely,  : 
of  llii-  corrMpondint-  sensory  e^nglion. 


t  can  be  felt  is  swollen  and  tender.     There  may  be  an  infianmiatory  focus  n 


The  pain  is  felt  above  the  eye  in  the  forehead,  i 
tender.     If  tension  of  eyeball  be  increased,  exan 


the  temple  and  s 

ue  ejt  for  glati.Dn 


or  tumor  involving  the  nerve  root  of  an  arm  or  especially  of  a  lev. 
r  back  as  the  vertex,     It  is  moat  severe  along  the  nerve  trunk  but  ectends  also  beyond   it  on  each  side.     The  tender  point  ; 


The 


f.    I.eprouB  oeuritia  (IHJU)  is  paiaU-^. 

I  of  pain  corresponds  to  the  distribution  of  the  fibres  of 


Neuroma   (4(>1). 

Compresiion  Neuritis. 

IliTpeliu  G.intfHonii is  or  Neuritis 

(H1-3-5-5I -8-06-88-94.  078.  1188.  1235). 

—V 

Neuritis   (489.  4itt.  834). 
Radiculitis. 


at  the  supra-orbitfll  notch.     The  eyeball  may  he  pnlnfal  and 


TIic  pain  is  felt  below  the  eye  in  the  cheek  and  sidi-  of  nose  and  radiates  into  the  teeth 

The  pain  Is  felt  in  the  lower  jaw  and  ita  teeth  and  gums  and  in  the  aide  ot  toneue,  in  the  ci 

The  pain  is  felt  in  two  or  three  of  the  eltnationa  described  above. 

The  pain  is  momentary  in  duration  and  is  associntofl  with  a  dtmii',  or  a  series  of  clonic,  spasi 


if  the  upper  jaw.     The  tender  point  is  at  the  infra-orbital  foramen. 

lie  car  and  in   the  temporal   rogion.     The  tender  points  are  at  the  me 


s  felt 


in  the  occipital  region  running  up  aloni  one  side   .it  the  scalp  to  liie  verli'x.    T*be  neck  Is  stiff.     T^c  tender  points  an'  bi'liind  lln'  innitoid  luvci 
arly  sjinplcm  in  neurasthenia  and  nerrmis  break  riown.     In  many  eases  the  pain  is  dull  and  is  a  sense  of  strong   prc'isure  raiher  than  poin. 


,  behind  the  middle  of  the  sterno-deido-maEtoid    muscle    and    on    the    parietal   eminence.     This  is  i 


Infra-orbital  Neuralgia  or  Neuritis. 
Infra -maxillary  Nenralgla  or  Neuritis. 
Trigeminal  Neunlds  or  Nearltis. 
Tic  DouIour«us  (fiOO). 
Ocdpllal  Neuralgia  or  Neuritis. 


reriodicnl  attacks  (often  occurring  at  menstrual  cpixA)  ot  sevre  i-i 
crania  nngio-paralyticn)  or  pallor,  coldness  and  dilated  impils  (Ik 
ilolor  or  sensory  aphasia  may  be  present  in  the  attsek.  as  well  a 
age  and  often  shows  a  direct  inheritance,     "Symptonuitic"  miiia 


Pain  of  great  intensity  in  a  smalt  spot  anywhere  ou  acalp  ivith  the  feelini;  as  it  a  nail  was  being  driven  tbrouifh  the  akull  at  tins  point.    'Die  region  is  tender.    Hysterical  symptoms  (■115)  mre  present. 


I'ain  may  be  felt  at  any  time  but  is  worse  in  evening  oi  night, 
quent.    Cranium  is  often  tender  at  points.     Pain  may 'be  due 


ir  oenirs  only  at  night,  or  in  the  early  morning  hou>«.     It  follows  no  nene  distrlbulioa  but  is  felt  over  a  amall  area  and  extends  overa  wider  and  wider  circle.     Argyll- Robertaon  phenomenon   Is  fre- 
o  periostitis.    Lumbar  puncture  may  show  lymphooytorfs  or  positive  Wnssermnnn.     Optic   neuritis   may   be   present. 


bend  or  body. 
Exogenetlc. 

Autn-genelic. 

(Cerebral  byiirren; 
Cerebral  anemia. 
n,-adnohi 


Frontal  headache  may  be  due  to  gastric  dyspepsia  and  constipatian,  ns  well  as  to  disease  of  the  eye  or  caries  of  teeth.  Occipital  headache  and  temporal  heaitacbe  may  be  due  to  disease 
to  pelvic  disease.  These  referred  pains  are  associatvl  with  hypiTnlceRin  of  skin  ot  same  region,  which  may  be  as  constant  and  imnort^int  vvmiilnms  nv  is  the  pain.  The  pain  of  eye 
howevin-.  should  not  be  nttacheil  to  those  referred  psins  in  diniotisis. 

("Occurs  after  the  ingestion  of  narcotics.     Does  not  conw  on  Itnmeiliatcly.  often  not  (ill  the  next  day. 

lOccuTB  as  the  result  of  breathing  for  hours  foul  air  in  UDveotllatod  ronms.  especially  if  patient  is  accustomed  to  pure  air.    Transitory. 

rOceurs  as  Uie  result  of  constipation,  espi^cinlly  where  the  bowels  usually  net  freely,    Tliis  headache  is  usually  most  marked  in  the  frontal  re;;ion. 


t  Occun  in  Bri):ht*s  disease,  usually  is  worse  when  patient  lirst  v 


Urine  Is  usually  scanty  and  contains  albumen  and  ea^^t^.     Kdcnm  and  gastric  dint  irbances  n 


Headache  with  fulness  and  throbViiug  In  hood,  acimivated  by  cough.    The  congestion  may  bo  active  (after  takinfr  amyl  nitrite)  or  pas* 
may  be  followed  hy  o  i^erehral  hemorrhage,     nendni^iM  occnrrinj;  at  the  lime  of  puberty  "r  of  menstruntion  may  well  he  eonjrestive. 


!  (heart  diseasel.    Vertigo  and  vomiting  may  he  present.    High  arterial  tensim 
iften  associated  with  albuminuria  and  occasionally  with  i-asts. 


Headache,  most  co 
posture.     In  this 


monly  at  vertex,  with   fnintintt,     Dsrkness  befcire  eyes,     fold  hands  and  feet.     Cardiac  or  arterial  disease  present,     A   series  of  such  headaches  may  be  followed  by  i 
as  in  other  forms  of  headache,  aevsrtl  etiological  fncinrs  may  be  present. 


iiri'-p 


issoctateil  with  phobias  and  tremors  and  inKomnIn  i 
williiu  the  akull,  eapeHally  preasore  in  oi-cipital  t 


mptomi  of  neurasthenia.    Pain  grows  less  t"ward«  evcnini;  and  is  iisimlly  felt  In  the  occiput  or  vertex.     Feeling  a 
region.    Headaches  resulting  from  ov  er  strain  (merilJil  or  physiral.  espwlnlly  eye  strain)  may  well  be  of  this  nntur 


it  a  tishi  band  i 


■crehral  thrombosis.      The 
re  upon  the  head  {cawiue 


Evidence  of  serious 
brain  disease.  Hesd- 
nehe  often  associated 
with  vomiting,  or  ver- 
tigo, or  both. 

Chronic  headache. 
Pain  constant  with 
cxBcerbatlons. 

Evid'^nce  of  infection. 


Optic  nenntu 
chofeed  disc. 


or 


IProcressive  nymploms,  motor  or  sensory  or  both,  first  of  irritation.  Inter  of  pantljTiis.     In  ease  of  abscess  there  may  he  n  latent  period  and.  in  llie  a 
over  the  seat  of  the  lesion.     Lumbar  puneliire  shows  greatly  In<'ren>red  pressure  of  cerehro -spinal  fluid.     Surfi  headaches  can  be  relieved  by  "ic 
Orebellar,  without  motor,  ataxia  Is  present.     Vertiiro.    Cerebellar  tits. 


■ver,     Heailanhe  v 
"dectimpression." 


.  is  iirton  present. 

TiiiiiituK  ;iuiiiiTn,     A   serie«  -if  surti  headaches 

hnndadic    may    be    relieved    by    the    recumbent 

neumsthcnlque).    Ofti'n  a  sense  of  fulness  and 

nir.'  .■a*es  the  vikiill  nia.v  lie  lenili-r  ..n  pi-r.-.i^ion 


Intractable,  incurable,  more  or  less  constant  headachw.    No  cause 
or  stretching  of  the  dura  mater  by  tumor,  hydrocepholus.  etc. 


Evidence    of    rheuma- 
tism elsewhere. 


DilTuse  pain  and  tenderness  of  scalp.    Pnin 
rTemporatj.  Occurs  during  the  first  few  days  or  But 

I  Pennanent, 


lie  n-sisned. 
r  may  be  pru 

movement  of  fronto-oecipital  muscle. 


Hay  he  e 


other  eereheal  '■ 


No  ..pii<-  1 


rili-..     I,u 


vill    I 


lally  vho- 


Evidence  of  exposure  to  hiRh  temperntu 


llI«torr  of  exposure  i 


Relieved  often  by  nppHcatlon  of  warmth.     At  times  siuat 
'k  of  almost  any  (ever   (typhoid).     Ruah  headaches  may  he  du"  lo  the  a.-ti 
Occurs  throughout  t*e  disease  and  Is  associated  with  muscle  spasm  and  paralysis  and  local  edema  of  tlie  scalp   (sinus 
Suppuration  elsewhere  In  head  er  body.     Latent  stage.     Convulsions  and  coma, 
high  temperature.     Headache  otten  folIowc-1  by  coma  and  convulsions. 


li'iiiler  nodules  can  he  fell,  and  hence  the  eondition  has  been  ca 
I  of  the  toxic  sulistanec  dir-'"tly  upon  the  brain  or  Indirecll.v 
irombosiH).     Coma.     Lumbar  puncture  will  show  tymphocytui 


nnphocytdsii!.      ,\popTeetic   attach'*    may 

lied  "indurative  headnehe." 

by  niiislne  vnao-pBralylic  congestion 

lis  and  globulin  in  cerebro-spinal  tluld. 


Trigeminal  9Vi 
Neuralgia 


iomeiimes  on  one  side,  sometimes  on  the  other  side  of  the  craniiun.  Skin  Is  very  hyperalgcsic  and  vaso-motor  disluihancea,  either  in  the  form  of  flushing,  sweating  and  contracted  pupils  (heml- 
-ania  aniiio-spasticn)  are  often  present.  Often  ushered  in  by  vlsunl  hallucinations  in  the  form  of  flashes  of  light,  speetrn.  etc.,  or  by  paralytic  phenomena,  such  ns  hemlanopia.  and  sootomata. 
insitory  local  paralyses,  especially  in  the  domain  of  the  cranial  nerve.«.  TowbrI*  the  end  of  the  attack  there  are  vomiting  and  nausea.  The  disease  usually  commences  in  early  life,  ceases  in  old 
is  not  intre<|uent  in  tabes,  paresis,  brain  tumor  and  epilepsy. 


Migraine  or  Hctnlcranla.     Idiopathic  and 
symptomatic    (8in,  )=FvS.  1020), 


of  the  eye,  ICPlh.  pharynx  or  ear.     Vertex  headache  may  be  due  to  anemia  or 
trail)  iirowsworse  mwards  evening,  or  follows  reading.     Too  much  importance. 


Ciavus,     Hysteria   (lOTfi). 
Syphilitic  Neurnlgin    (meningitis). 

Referred   Pains  nr  Rymplomatie  Neurnlria 
(374). 

AlcDhelic  or  Mini>hine   Ilendndie. 

Foul  Air  Headache, 

Constipation  Headache. 

Uremic  Hsadache. 

Congestive  and  High  Teusion   Headache. 

Anemic  Headache, 

Neurasthenic  Headadie  (IflTll. 

rerebral  Tumor,  or  Abv.-pwi,  or  Hydrocephal 
(HOT.  1506,967). 

r.T-lv-llar  Tumi.r   (Il«l!H  , 

PachymeBinptls  and  (^ir..nic  Meningitis 
(588,  S90). 

Rheumatism  of  Scalp. 

Infectious  or  Toxic  Hendaelie. 

.Icute  Uenlnptis  and  Sinns  l^romhoals  (590,] 

Cerebral  AbsceM  (961). 

Sunstroke    (G8».  1070). 


CHART XVb 

Pain  in  Trunk 

Comprising  Numbers  935  on  left  side  of  Chart 
and  970  to  991  on  right  margin 


189 


DIAGNOSTIC    SYMPTOMS    AND    TESTS 


DIAGNOSTIC   ANALYSIS 
PAIN  IN  TRU: 

ABSTRACT    01-     SYJ 


f  Evidence  of    rPain     and     tender- r  l'liubi;is  aud  nervous  oxiuiuslion,  paiu  and  sense  of  pressure  most  marked 
neurotic 
tempera- 
ment.    No 
evidence  of 
organic 
disease. 


Pain  in  back." 


935 

PAIN   IN 
TRUNK  IN 
NIi;RVOUS 
DISEASES. 


Pain  in 

thorax  and 
abdomen. 


uess       of      spinousJ 

processes.  [Hysterical  symptoms   (llfi).     Much  tenderness  of  spinous  processes,  espei 

Pain     and     tender-    Severe  pain  in  coccyx  witliout  evidence  of  any  disease  of  it.     Pain  iucreas 


.ness  of  coccyx. 


Evidence  of 

organic 

disease. 

Pain,  tender-    May    follow 

ness  and  traumatism. 

rigidity  of 

spine. 


Vertebral  ciilumn 
is   ankylosed. 


Unilateral. 


bysterical  symptoms  (415)  are  present. 


Severe  and  constant  piiin  in  back  and  radiating  about  body  and  into  extrcm 
-Mucb  spasm  of  spinal  muscles.  Exag-gerated  reflexes.  Little  or  no  para 
and  if  any,  it  is  of  a  transitory  nature.     Hyperesthesia  and  hyperalgesia 


Slowly  increasing  motor  and  sensory  symptoms,  irritative  and  paralytic 
iugeal,  when  paralytic  symptoms  are  more  prominent,  the  tumor  is  in  th( 
more  girdle  pain  aud  pain  radiating  into  extremities  than  in  meningitis 

It  may  be  possible  to  feel   exostoses  on  vertebrae.     Unilateral  or  bilateri 
lesions  in   other   parts   of   the   body.     X-ray   examination   makes   the   c 


Girdle     pain 
(374). 


No      other      symp- 
toms. 


Many   other  symp- 
toms. 


Bilateral    usually.  - 


No      other      symp- 
toms. 


.\t  first  unilateral  and  later  bilateral. 


In  mammary 
gland. 


Hysterical       symp- 
toms. 


Dhl    age. 
disease. 


.Arterial 


In     prccordia     and- 
arm. 


.\ny  age.  No  arter- 
ial disease. 


Pain  shoots  around  chest,  following  the  course  of  an  i 
costal  nerve,  Or  may  be  limited  to  a  small  area  o 
nene :  pleurisy,  pericarditis,  pneumonia,  pleurod 
periostitis,  etc..  having  been  excluded  by  a  careft 
amination. 


Loss    of    knee-jerk.      Argyll-Robertson    phenomi-non. 
syphilitic  infection. 

There  is  a  zone  of  hyi)erosthesia  where  the  girdle  pa 
may  be  severe. 

History  of  other  evidence  of  syphilis.      Lumbar  pui 


Slowly  increasing  motor  and  sensory  symptoms,  at  fii 

Paroxysmal  attacks  of  pain  in  one  mammary  gland, 
gland  can  be  detected.     Pain  is  usually  in  the  left 

Paroxysmal  attacks  of  pain  in  precordia  shooting  u 
in  sternal  regicm.  of  suffocation  and  impending  de 

Pain  similar  to  the  above,  but  no  arterial  disease, 
gestion,  tobacco,  overwork,  etc.     Not  infre<iuentlj 
quently  than  does  true  angina. 


Local  pain. 


Along     attadiment    I'ain  felt  in  lower  anterior  part  of  ohest,  also  in  same  side  of  neck,  most  fr 
of  diaphragm.  xysms.     Tender  points  are  along  tlie  attachment  of  tlie  diaphragm  and 

ease.     An  extremely  rare  disease. 


In  abdomen.  In 
all  these  rare  forms 
of  neuralgia  organ- 
ic abdominal  dis- 
ease must  be  care- 
fully and  thorough- 
ly excluded. 


In  genitals. 


■Paroxysmal  attacks  of  pain  in  epig.ostrium  ufii-n  ncruiTiug  at   rlin  same  h( 
of  stomach  or  neighboring  viscera,  especially  no  gall  stones.     May  be  ai 

Similar  paroxysmal  attacks  of  severe  pain,  occurring  irregularly  at  pylo; 

Paroxysmal  attacks  of  severr  pain  in  abdonii'u  occurring  with  some  perio( 
been  excluded.    Pain  relieved  by  pressure.    Blue  line  on  edge  of  gums, 

.Pain  in  hip,  groin,  hypogastrium  and  genitals.     Tender  points  near  spine. 

Neuralgic  pains  and  irritability  in  the  pelvic  viscera,  the  bladder,  rectum 
Neuralgic  pains  at  times  occur  during  years  in  one  testicle  or  one  labiui 


SYMPTOMS 


roMS 

cervical  spiue  and  occiput. 

l.v  in  mid-dorsal  region ;  ovarian  ti'iKierncss  is  also  common. 


DIAGNOSIS 

Neurasthenia    (1074). 


970 


Hysteria.        Spinal      Neu-     971 
ralgia   (1076). 


jy  motion,  touch,  defecation,  etc.     In  most  cases  there  is  a  history  of  injury.     Often       Coccygodynia. 


972 


Injury.     Very  sudden  onset.     Lumbar  puncture  may  show  bloody  fluid.     Rptention 
of  urine. 

History  of  iut'ectiou  (septic,  syphilis,  etc.).     Lumbar  puncture  shows  globulin  and 
increase  of  cellular  elements  in  cerebro-spinal  fluid. 

raplegia  dolorosa).  Wiien  irritative  symptoms  are  very  prominent  the  tumor  is  men- 
rd.  Symptoms  at  tiret  usually  unilateral,  later  bilateral.  Less  pain  and  spasm  in  back, 
lally. 

irdle  pains  at  level  ol  the  disease.  Rarely  any  paralytic  symptoms.  Usually  bone 
uo.sis  positive. 


Tender  points  of  Vallei.x :  one,  two  iucies  from  pi^terior  median  line ;  another, 
two  inches  from  anterior  median  line;  and  a  third,  in  mid-axillary  line.  Other 
points  on  nerve  may  also  be  hyperalgesic.  Pain  is  paroxysmal.  Respiration, 
cough,  sneezing,  etc.,  are  painful. 

Rash  of  herpetic  vesicles  along  eouisi  of  nerve.  Rarely  associated  with  motor  or 
sensory  paralysis. 

/umbar  puncture  gives  lymphocytosis.  Ataxia.  Lightning  pains  in  legs.  History  of 
s  and  below  a  bilateral  anesthesia,  which  may  be  slight,  and  a  motor  paralysis,  which 
re  gives  lymphocytosis.     Pains  worse  at  night. 


Hematorrhachis   (524,  973 

(W.). 
.Meningitis  Spinalis,   acute     974 
( febrile  1      and     chronic 

(afebrile)      (60.5,    1005, 

1213-4). 
Spinal   Tumor    (.509,   826.     975 

S.S9-44.  9,S2,  1006). 

(Figs.  24-7). 

Spondylitis        Deformans.     976 
.\rthritis    Deformans. 

Intercostal  Neuralgia.  977 


Herpetic    Ganglionitis  or      97S 

Neuritis  (940,  1166,  1235). 

Tabes    (661,   829).  979 
(Fig.  27). 

Transverse  Myelitis.  9S0 
(Figs.  24-7). 

Syphilitic    Meningitis.  981 


rritative,  later  paralytic.     Hrown-S^quard's  paralysis  at  first   (432). 


Spinal    Tumor    (975). 


1,  at  times,  radiating  beyond  the  limits  of  tlie  breast.     No  tumor  or  other  disease  of  the       Mastydynia. 
ist. 

left  shoulder  and  even  down  left  arm  and,  at  times,  both  arms.     Sense  of  oppression       Angina  Pectoris- 
Arterial  tension  is  usually  high.    Area  of  cardiac  dulness  usually  increased. 

■urotic  individual  who  has  an  overstrained  heart.     At  times  tiie  result  of  gastric  indi-       Pseudo-.\ngina    Pectoris. 
!  result  of  an  adjacent,  dry  pleurisy  with  well-marked  friction  rub.     Occurs  more  fre- 


982 
983 

984 

9S5 


;ntly  on   left  side.     Breathing,  sneezing,   coughing,  etc..   painful.      Pain   occurs   in   paro-       Phrenic    Nouralu'i: 
lind  sterno-eleido-mastoid  muscle.     No  sign  of  pulmonary,  pleural,  cardiac  or  other  dis- 


986 


especially  in  the  early  morning.     No  digestive  disturbances  or  evidence  of  any  disease       Gastralgia. 
ated  witli  (ontraclion  of  the  empt.v  stomach  and  consequent  feeling  of  hunger. 


or  neck  of  bladder  or  anus,  associated  with  symptoms  of  tabes   (661). 


987 


Tabetic  Crises  (423.  829).     988 


y,  when  biliary,  renal  and  other  forms  of  colic,  appendicitis,  diverticulitis,  etc..  have       Bnteralgia    (Lead    Colic.        989 
3t-drop,  lead  in  urine  after  adniinistraticn  of  K.  I.  etc.). 

;rest  of  ilium,  inner  part  of  groin,  etc.  Ijumbo  -  abdominal      Neu-     990 

ralgia. 
srus.  vagina   and    uiotlira.    but    these    ar.-    rare    and    relatively    unimportant    conditions, 
ijus.     From  this  point  the  pain  may  radiate.  Pelvic  Neuralgia.  991 


CHART  XVc 

Pain  in  Extremities 

Comprising  Numbers  936  on  left  side  of  Chart 

and  995  to  1012  on  right  margin 


191 


DIAGNOSTIC    SYMPTOMS    AND    TESTS 

I'aiu   in  arm. 


Pain  limited  to  the 
tnmk  and  distribu- 
tion of  the  sciatic, 
anterior  crural  or 
oliturator  nerve. 


Pain   limited   tn 
outer   surface   of 


936 

PAIN  IN 
EXTREMITIES 
IN  NERVOUS 
DISEIASES. 


(•Unilateral.       Many 
of    tliese    forms    of 
neuritis  may  be  as- 
sociated    with,     or 
precede,    or    follow]  ""'"• 
a   rash   of   herpes  ilp^i^  ;„  „  ^^-^^^^ 
herpetic  ganglio- 
nitis. 

(Figs.  33.  38).  Pain  at  insertion  of 

Achilles'   tendon. 

Pain  in  heel. 
Pain  in  toe. 
I  Burning  pains. 


DIAGNOSTIC   ANALYS 

PAIN  m  EXllE 

ABSTRACT   OF 

I'.iiu  radiates  along  one  or  all  of  the  nerves  of  tbe  arm.  Tender  pc 
other  points  where  nerves  are  supei-ficial.  Vaso-motor  disturb;i 
paralysis ;  but  movements  of  arm  are  impaired  by  the  pain.  Turn 
pressure  on  nerves,  must  be  carefully  excluded. 

C  Pain  shooting  along  the  trunk,  or  over  small  areas  in  the  distribi 
y.><is,  but  the  pain  may  prevent  motion.  Patient  holds  knee  of  t 
body  to  the  opposite  side  and  bears  his  weight  on  tlie  healthy  leg. 
trucbanter  major  (trochanteric  point)  and  in  popliteal  space  (p 
and,  then,  there  may  be  decided  muscular  weakness  and  atrophy, 
rectal  exaraiuatiou  for  any  possible  pressure  upon  tbe  nerve  sho 
in  Sciatic  neuritis. 

Pain  along  tbe  trunk  and  distribution  of  the  anterior  crural  nerve 
ankle.  Tender  points  on  anterior  aspect  of  the  hip  joint,  inner  : 
paralysed  and  atrophied  and  knee-jerk  lest  and  anesthesia  may  b 
be  secondary  to  diabetes  and  injury.     There  may  be  an  eruption 

Pain  along  inner  side  of  thigh,  along  course  of  obturator  nerve,  afi 
neuralgia  and  is  usually  associated  with  paralysis  of  the  adduci 

Pain  is  associated  with  paresthesiae  (especially  numbness  and  tinglj 
Hat  fooi  or  weakened  arch.  The  paresthesiae  are  more  charact', 
absent.  , 

Pain  in  a  joint,  usually  the  knee-joint,  increased  on  motion.  The  -1 
dence  oi  any  disease  of  the  joint.     Many  hysterical  symptoms  (i 

Sevei'e  pu.n  at  insertion  of  Achilles'  tendon  on  walking  and  stand ii 


Bilateral. 


With  girdle  pains, 
and   lumbar  punc- 
liire   gives 
lymphocytosis. 


With    anesthesia. 


With  dissociation 
of  sensation. 


With   vaso-motor 
disturbances. 


I  With  fat. 


Pain  in  lower  surface  of  heel,  especially  when  walking  or  standing,  t 
gical  removal  of  the  sub-calcaneal  bursa,  or  of  exostoses,  others  b 

Pain  in  the  metatarso-phalangeal  joint,  especially  of  the  fourth  toe,  u 
is  lowered  from  "breaking"  of  the  arch  transversely. 

Intense  burning  pain,  usually  in  foot  or  hand,  often  associated  withh; 
nerxe  injury  which  is  not  complete.    At  times  due  to  flat  foot. 

"With  Romberg's  symptom,  Argyll-Robertson's  phenomenon,  ataxia,  h 
lymphocytosis  and  lightning  pains  over  small  areas  in  legs,  super 

With  pain  and  rigidity  in  back  and  in  extremities.  Exaggerated  refi 
cocytosis  or  lymphocytosis  in  cerebro-spinal  fluid.  In  cases  in  wl 
dolorosa"  may  result. 

Steadily  progressive  motor  and  sensory  symptoms,  at  first  mainly  u 
fluid.     Brown-Sequani's  paralysis  (432). 

Motor  paralysis  and  anesthesia  over  whole  of  both  legs,  except  in  sc 
peripheral  and  organic  reflexes.  Muscular  .itrophy  and  trophic  di 
in  lower  back  and  radiating  into  legs. 

Motor  and  sensory  paralysis  commencing  at  the  distal  end  of  extremi 
and   tenderness.     The  di.seasc   usually  commences  with   pain  or  p: 

Pain  and  paresthesiae,  analgesia  and  thermic  anesthesia  without  t; 
symptoms  are  usually  limited  to  ai-ms  with  symptoms  of  spastic  p; 
but  are  milder. 

ICxtreme  pain  in  soles  of  feet  associated  with  redne.ss  and  swelling  an 
Flat  foot  must  be  excluded. 

Pallor  and  coldness  of  fingers  and  toes  followed  by  cyanosis  and  cong^ 
In  extreme  cases  a  larger  or  smaller  slough  forms  and  is  cast  off. 

Marked  increase  in  fat,  cither  diffuse  or  in  separate  tumors,  in  arms 
ated  with  it,  and  the  fatty  masses  are  tender,  especially  in  the  ea 


OF  SYMPTOMS 
SMITIES 
MPTOMS 


DIAGNOSIS 


^""S^r^^S  ir  Uu;i!r'ol?^''^.?L:t'I'^t:^      V,.r^<p^..^>^  Neuralgia  o.  Neuritis  of  Ulnar,  00. 

at  base  of  neck  and  in  axilla,  and  a  ce'ical  tti^^^    o-^^in^  oltl^S:       '  ''"'  ''"""""''  '"  ""  '"^t"'^>'«- 


99(i 


a  of  the  sciatic  nerve.    Little,  if  any,  anesthesia  or  motor  paral-       Sei-itici    (T^O) 

affected   side  semi-flexed,   thigh   slightly   abducted,   inclines  his  '      '    '  "   '" 

-ender  points  over  the  sciatic  notuh  (gluteal  point),  above  the 
Ileal  point).  In  neuritis,  the  nerve,  wherever  felt,  is  tender, 
i-ialica  is  mueh  more  frequently  a  ueiiritis  than  a  neuralgia.    A 

always  be  made.     The  tendo  Aebillis  reflex  is  often  abolished 

the  anterio.  surface  of  the  thigh  and  inner  surface  of  leg  to  the      fnirnl  Neuralgia  or  Neuritis  .v.- 

■  ot  knee  and  at  internal  malleolu.s.     Extensors  of  thigh  may  be  '^'ni.u^m  oi   i>Lunti.s.  .).), 

anterior  surface  of  thigh  and  inner  side  of  leg  in  neuritis.  May 
herpes  along  the  course  of  the  nerve. 

hernia  and  other  diseases  have  been  excluded.     A  rare  form  of      Obturator  Neuralgia. 


99S 
999 


1003 
1003a 


t'""l  ^  Probab./  always  associated   with,   and  is  caused   by,  Meral»ia   Paresthetica 

pic  of  this  disease   than  is  the   pain,   which   is   often   entirely  '''"°^''   ^  iiestnetica. 
I 

Us  much  more  sensitive  than  Uie  articular  surface.     No  evi-  Arthralgia  „r  Hysterical  .Tuint.  1000 

May  follow  gonorrhea,  malaria,  gout,  broken  arches  or  injury.  AchiUodyuia.  lOQ] 

e  cases  are  cured  by  anti-rheumatic  medicine,  others  by  sur-  Talalgia  or  Calcanodvnii  irMV> 

upporting  the  weakened  arches.  laiai^ia  oi  Laicanofiynia.  1002 

lly  following  an  injury.     Usually  occurs  in  women.    The  joint  Mela  tarsalgia  or  Morton's  Too. 

•hidrosis   and    vaso-motor   disturbances.      Usually    caused    by  Causalgia  or  Thermalgia. 

ry  of  syphilis  usually,  always  loss  of  knee-jerk,  cerebro-spinal  Tabes      Neur.iKic  sta-e   (a^^)  1lv^A 

1  and  deep,  often  followed  by  hyperalgesia  over  same  area.  -XemaUic  sta^e   ((,(,]).  1004 

'nu^rj!'^'^''''      ^,°    Argyll-Robertson's    phenomenon.      I.eu-  Spinal  Meningitis   (GOT.,  !)74,  120,-!^)  lOOT 
the  cord  is  secondarily  compressed  or  involved  "paraplegia 

teral,   later   bilateral.      Increased    pressure   of   cerebro-spinal  Spinal  Tumor   (509.  82S,  839-44,  97.5).  1006 

eases  the  domain  of  the  anterior  crural  nerves.     Abolition  of  Lesions  of  Cauda  Equina    (487)       (Fig  29  )             1007 

b.inces.     Anesthesia  in  perineum  and  genitals  and  much  pain  (rig.  „i.i              jihi, 

and  extending  towards  body.     Muscular  weakness,  atrophy  Multiple  Neuritis   (488)  inos 

lesiae  in  toes  and  fingers  and  often  with  fever.  -^euu^s   ^*^^,).  lOOS 

•  anesthesia.    Trophic  disturbances  and   mutilations.    These  Syringomyelia    (553    093    840-"    115"    1170    11S7      1000 

r,'ia  in  legs.     The  pains  often  resemble  the  pains  of  tabes,  1370-2) 

er  with  pallor,  shrinking  and  wrinkling  of  the  same  parts.  Erythromelalgia    (1198).  10l5 

n:  so  that  fingers  and  toes  become  purplish  and  even  bl.-ick.  Kaynaud's  Disease   (1195).  1011 

.ages  ':lrL:lZ':7:rJ'r  '^  ™"^"''^''^'^"-  ""■"  "-^«""-  -^"'P--  D°'—  Dercum-s  Disease   (1175).  1012 


CHART XVd 

Vertigo 


Comprising  Numbers  932  on  left  side  of  Cliart 
and  1015  to  1034  on  right  margin 


193 


DIAGNOSTIC    SYMPTOMS    AND    TESTS 
Motor  Ataxia   is  present. 


Cerebellar  Ataxia  is  present 


932 


B 
T 
I 
G 
O 

(392) 


Crossed  Paralysis. 


Vertiao  on   niovoincnt  of  lieaj. 


Di'afiHss  .iiiil   syni|il(iiiis  nf  aural  diseasp. 


l>iliN>lii:i  niKl  symptoms  of  ocular  disease. 


Position  and 
nujving^ 


Symptoms  of  cir- 
culatory or  digest- 
ive  disturbances. 


I'xliaustion. 

Digestive  dis- 
orders. 


Cardiac  and  hemic 
disease. 


.Vtlieromatous 
arteries. 

High   blood 
tension. 


Aiir)plexy. 
Rpilepsy. 

Migraine. 


Toxic. 


Symptoms  of 
cerebral  disease 
(headache,  etc.). 


Organic. 


Functional. 


DIAGNOSTIC  ANALYSIS   OF 

DISORDERS  OF  SENSATION;  PERV] 

ABSTRACT  OF  SYMPl 

In  tlicse  cases  the  vertigo  is  not  a  prominent  symptom.  In  some  cases,  iu  consc' 
of  falling  and  fears  that  he  will  fall  and  experiences  some  vertigo  ;  while  in  oth 
lesions  in  the  brain  stem  and  elsewhere.    The  diagnosis  is  made  from  the  pres 

Any  disease  of  the  cerebellum,  especially  tumors,  may  cause  vertigo,  which  is  m 
of  the  hemispheres.    The  diagnosis  is  made  from  the  absence  of  paralysis,  the 
and,  in  tumors,  the  optic  neuritis  and  failure  of  sight. 

Lesions  of  tlie  brain  stem  may  involve  the  tracts  from  the  cerebellum  and  cause 
made  by  the  motor  or  sensory  paralysis  or  both,  which  occurs  in  the  form  of  1 
paralysis  in  the  domain  of  the  cranial  nerves  (crossed  paralysis,  etc.).     (B'igs. 

Cysts  and  tumors  suspended  free  in  the  fourth  ventricle  cause  intense  dizziness  t 
drome).  Except  for  this  symptom  the  diagnosis  is  e-xtromely  difficult  or  impossi 
the  position  in  which  the  head  is  held.     Choked  disc  is  common. 

.\  steadily,  progressive  deafness  of  one  car  associated  with  tinnitus  in  that  ear,  a 
may  throw  patient  to  the  ground.  Kaisiug  the  head  from  the  ground  may  cau: 
or  loss  of  bone  conduction  and  loss  of  power  of  hearing  high  notes  are  usually 
the  paro.\ysmal  attacks.  Suppurative  and  other  diseases  of  the  ear  may  be  p 
when  the  ear  is  completely  deaf,  but  then  may  commence  in  the  other  ear.  Alt 
may  cause  vertigo  by  affecting  the  semi-circular  canals  or  vestibular  nerve  dii 
laesa).  It  is  difficult  to  draw  the  line  between  these  cases  of  aural  vertigo 
cover  all  these  conditions.  Strictly  speaking  Meniere's  disease  apiilies  only  to  a 
Uammation  of  the  labyrinth  causing  vertigo  is  called   Voltoni's  disease. 

D.Hible  vision  and  weakness  of  ocular  muscles  and  eye  strain  may  cause  vertigo. 
IS  relieved  by  closing  the  defective  eye,  even  when  it  is  not  caused  by  the  dip! 

When  patient's  head  is  bent  down  for  a  long  time  and  then  is  suddenly  raised, ' 
enees  vertigo.  A  blow  on  the  head  will  cause  vertigo,  probably  in  consequeuci 
of  back  of  head  or  moving  head  quickly  may  cause  vertigo.  A  similar  vertigf 
rent  to  the  head. 

Great  weakness,  especially  in  the  convalescence  from  disease,  is  a  common  cause 

When,  iu  cousefjuence  of  the  congestion  due  to  digestive  disorders,  the  portal  ciiN 
aie  anemic.  These  digestive  disorders  may  also  produce  abnormal  chemical  s 
diagnosis  is  made  by  the  presence  of  the  digestive  disorder  and  by  the  cure  of 

In  all  forms  of  cardiac  disease  the  brain  may  receive  an  insullicient  and  irregular  : 
frequent  in  aortic  disease.  The  diagnosis  is  made  from  the  presence  of  cardiac 
to  the  altered  quality  than  quantity  of  the  blood  supply   (1030). 

Atheromatous  arteries  interfere  with  the  normal  blood  supply  both  as  to  amount 
cause  vertigo.    This  is  especially  common  in  elderly  people.    The  diagnosis  is  m; 
usually,  an  increased  arterial  tension. 

Fulness  of  head,  headache,  mental  confusion,  tinnitus  aurium,  palpitation  of  hen 

\'ertigo  is  a  common  initial  symptom  of  apoplexy  of  all  forms  (ccr'bral  hemorrha 
rhage)  and  may  be  the  only  symptom  of  a  slight  attack.    Usually  the  sequence  o 

\'ertigo  may  constitute  the  aura  which  may  or  may  not  be  followed  by  a  full  at 
tiicks.  In  some  cases  a  severe  subjective  sensation  of  vertigo,  frequently  foUowc 
attack.    Vertigo  is  not  an  uncommon  symptom  in  the  interval  between  the  atta 

Vertigo  may  be  the  initial  symptom  or  may  accompany  an  attack  of  migraine.  Th 
makes  the  diagnosis  plain. 

I  Abnormal  conditions  of  the  blood,  as  in  Uie  early  stages  of  infectious  diseases  a 


I 


Various  toxic  substances,  such  as  tobacco,  alcohol,  coffee,  morphia,  <iuiuine,  etc.,  v 
tion  of  the  cerebral  or  cerebellar  cortex.  The  diagnosis  is  made  by  the  proof  of 
vertigo. 

A  disease  endemic  in  Switzerland  and  occurring  only  in  men  working  in  hot  cow 
ness  of  vision,  ptosis,  often  diplopia  witliout  strabismus,  and  a  iiaralysis  of  son 
Pain  in  back  of  neck.     Attack  lasts  a  few  minutes. 

In  addition  to  apoplexy,  any  irritation  of  the  meninges  (tumors,  local  lesions  andi 
associated  with  severe  vertigo,  especially  on  cliange  of  position.     Tumors  may 
mitted  pressure  on  the  cerebellum,  or,  when  situated  in  the  frontal  lobe,  by  dii 
diagnosis  is  made  by  the  numerous  other  symptoms  of  these  dis. ascs :  convulsic 
associated  with  the  vertigo,  which  is  less  severe  in  the  recumbent  i)nsture. 

Vertigo  is  not  an  uncommon  symptom  in  those  functional  nervous  diseases  which 
chronic,  such  as  neurasthenia,  the  traumatic  neuroses  and  hysteria.  The  diPfe 
This  vertigo  is  never  very  severe  and  often  rather  resemble  syncopal  attacks. 


MPTOMS 
sION;  VERTIGO 

[S 


DIAGNOSIS 


.ce  ui;  tie  iucoGrdinatioii,  tlie  patient  is  in  danger      t^i,^      Disseminated   Sclerosis  and   other  disease.     1015 
eases  tlie  vertigo  may  be  tlie  diMct  result  of  the  ^^jUj  ^^.^■^]^ 

i  of  motor  ataxia.  ..... 

permanent  in  lesions  of  the  vermis  than  in  those      Cerebellar  Disease    (3»2,  r,07-S-47-SC,   'fH.  129.^).     1016 
ience  of  cerebellar  ataxia,  headache,  and  vomiting 

da  and,  less  frequenUy,  vertigo.     The  diagnosis  is      ,^,,^i„„,  „f  t,,^,  ,„,„;,,  ,t^^    (400,  r,a5-4t!.  C.m.  832,     1017 
iplegia  with  increased  redeivs,  and  also  by  local  l21K)-7    1321-4    1387-90-4.<!    1400-8). 

,  or  mainly,  when  head  is  moved.      (Krtin's  syn-      ,,,;„„,  .^.i,,,;,,  ,.,,^,  f,,,,,.^,  ventiicle   (Fig.  19).  lOlS 

Ihe  vertigo  may  vary  greatly  in  intensity  with 

nith  paroxysmal  attacks  of  severe  vertigo  which       Meniere's   Disease.      Volloni's   Disease.      Aural  101!) 

oniuing.     Attacks  vary  in  severity.     Impairment  ^.^^^.^^     ^.^,.^i       .,,^  ^^^,,.^  ,^^.^^,   (M0,(kS5,  MS). 

nt.     vertigo   is   usually  entirely   absent   between 

nt,  but  usually  are  not.     Disease  usually  ceases 

;  any  disease  or  functional  disturbance  of  the  ear 

y  or  indirectly  (aural  vertigo  or  vertigo  ab  aure 

Meniere's  disease,  which  latter  is  often  used  to 

of  hemorrhage  into  the  semi-circular  canals.    In- 

icurs  sometimes  on  railway  trains.     The  vertigo      „,    ,       y      ■         y    ^.      ^^  ^     ,^  1^^^„  (C^g)  io20 

I  alone.  o  -^ 

ehen  patient's  body  is  rotated  mpidly,  he  experi-      ^,.,,„.  ,-.,.rebral  Anemia.  1021 

vaso-motor  rellex  disturbance.  Lying  on  one  side 
;y  result  fii>m  tlie  application  of  a  galvanic  cur- 


h  of  vertigo  and  ataxia. 


Exhaustion   Vertigo.  1022 


tiou  is  engorged  with  blood,  the  cerebral  vessels  ^^^^^   Cerebral   Anemia   from   digestive   disorders,     1023 

.ances  which  rn^iy  produce  a  toxic  vertigo.     The  j^j.,,.,,,^,  hemorrhage,  etc. 
vertigo  when  the  indigestion  is  cured. 

ily  of  blood  and  vertigo  may  result.    This  is  most  cin-ovAc  Cerebral  Anemia  from  bl„n<|  :,„,!  cardiac     1024 

}ase.     In  hemic  diseases  tlie  vertigo  is  aue  rather  j. 

siseases.- 

as  to  uniformity  of  distribution  and  hence  may  Chronic  Cerebral  Anemia  from  atheromatous  nrfer-     1025 

linm  the  presence  of  atheromatous  arteries  with,  •  „  /^..^i-r.-e, 

Its     ^  Sjr  pll  1 1  lb  _)  . 

Jyspnoea  on  exertion,  and  high  blood  tension.  Cerebral  Congestion.                                                           ]02« 

embolism  and  thrombosis,  and  meningeal  hcmor-  .        ,  ,.  .    t-rn\                                                                   ii'io? 
her  symptoms  makes  the  diagnosis  clear. 

.    The  diagnosis  is  m.ide  from  the  epileptic  at-  ,.:,,i],.pgv    (57.-,,  lOCl,  1073).                                             102.S 

'  vomiting,  may  be  the  equivalent  of  an  epileptic  '      >    -     ^ 
and  may  continue  during  minutes  or  hours. 

micrania,   the   much   more   prominent  symptom,  :\[if;i.aine    (S49-.5S.  950).                                                    102S 

n  leukemia,  melanemia,  gout,  diabetes,  etc.  t^^j^  y„.y„„   (io24).                                                        1030 

cause  vertigo,  probably  by  aflceting  the  oircula-  jy         Vertigo                                    •                                    1031 
ingestion  of  the  substances  before  each  attack  of 

lies     It  consi.sts  in  attacks  of  vertigo,  with  dim-  Gerlier's  Vertigo.     Vertige  Pnralvsant.                          1032 
unction  or  act  of  the  arms,  simulating  hysteria. 

iecially  inflammations  and  syphilitic  lesions)    is  Cer,>hral  Meningitis  an.l  Tumor   (Syphilis)    (.%OS,       1033 

both  by  irritation  of  the  meninges  and  by  trans-  530-42) 

irritation  of  the  cerebro-cerebellar  tract.     The 

vomiting,  slow  pulse,  etc.,  which  are  frequently 

B    the    result    of    psychic    traumata,    acute    and  Neurasthenia.   Traumatic   Neuroses  an<I   Hysteria        1034 

lal  diagnosis  of  these  is  made  in  other  charts.  (1074-7). 


CHART  XVI 


Disorders  of  Cerebral  Activity 


DIAGNOSTIC  ANALYSIS  OF  SYMPTOMS 


Symptoms 

Alterations  in 

Analysed 

Mentality 

1037 
Coma. 

See  Chart  XVIa. 

1038 
Pseudo-Coma. 

1036 
Disordered 

Mentality. 

1039 

Double  Personality. 

1040 

Weakened  Mentality. 

See  Chart  XVIb 

1041 
.  Insanity. 

See  Chart  XVIc 

195 


CHART  XVIa 
Coma 


Coniprisint,'  Numliers  1037  on  left  side  of  Chart 
and  1042  to  1070  on  liijlit  margin 


197 


niAGNOSTKT   SYMPTOMS    AND    TESTS 


COMA  OR 

be:mi-coma 

(2I».745). 

Sm  abo 
Iifeado-coron, 

(inss). 


n-sidcnoe  in 
Alio  malnrEal 
malnrial  rcdoo*. 
•Ii>riii£  sod  after 


Bbtorr,    Of    oUier 

iTid^ncc   of    rt'Ci-nt      fV)nviil»itinii  rare. 

injur;  to  bead. 


f  I'lipils       imiinlly       crtDtmcrrc 
i      reapoud  heiHy  to  llsbt. 


Pupils    dilated.     ofU-n     unoqual,    i 
'      uBuallf  do  not  respond  to  light. 


T'nlicnl  iiiKy  In-  i-omiilrtoly  uiir..n«diiui  for  n  s'l"'''  tune,  nflor  wbidi  lie  r.'in/iit 
Symptoms  follow    thi'  Injury  iomrflately-     Rnroly  any   pnralysla.    Ofti-u  i 


DIAGNOSTIC    ANALYSIS   OF   SYKPTOMS 
ABSTRACT    OP    SYMPTOMS 
1  n  ilaioil  oondilioD  for  a  time,  or  he  may  be  onlyl;!'! 


May   bi'   conttiriun    of  scalp. 


Minx  iisunlly  M\<> 
I  symptnuiM,     Ofi 


tlif  iiijiirj  iininHli"i'^l>~'  but  flot  Alnnys;  thi>r.>  luiiy  in-  it  '■IuckI  intTvnl."   («s|iPdnUy  in  extra-dura!  hemorrliiiE^l.     Profound  comii,  aterlnmus  liri>atliing,  puls^  slow,  refl>ii<>9  :itiM|isbfd.  iiicrpnsod  irnaion  of  ccrebro-spiaal  fluid  b 
T  ponjiii:in»  dcvialinn  of  the  hoad  and  eyes.     Ofifii  piiriilynin  in  rlic  form  of  more  or  li-BS  complete  hemiplegia,  t^it'ltier  witli   Baliiuski  reflcv  ami  some  ^tinrai.     Often  relrogniile  umuc^ft   (772). 


ConvuIaiODS       a  r  p 
frequently   preaont. 


Thr  aymploma  an-  Ib-'w  of  n  Iol'oI  mcoincitis  (507,  1048)  or  obscess  (50*^,  1(H9)  wlHi  innnlly  hieli  fever  and  chills  (both  may  be  abaenti  occurring  in  n  cachectic,  anemic,  or  Snfcclfd  patient,  eBpecinlly  in  one  with  carie*  of  bone  of  skull  (otiliil.  Ileadsebc,  vomiting.  n<iitlc«ni'!W  and  delirium  prvccdlnq 
the  cnma  arc  common.  Tbcrc  may  be  loi-nl  syinptome.  both  irritative  niid  paralr'i''  -^  "^^y  ebnraclcristic  symptom  Js  a  localized  pilema  of  the  ^calp.  In  lhr(>u>lir»i8  of  superior  longilMdiunl  sinus  there  may  be  epistazlB  miil  nicma  in  root  of  nimc.  \Micn  Ihe  cnvemous  sinus  is  involved  thew 
may  be  cirma  of  eyelids  and  conjunclivar-.  diohod  di^cs.  prominence  of  (he«y«ball«  "H'l  oculo-motor  nnd  abduccns  pnralysis.    When  the  transverse  sinun  itt  involved  there  may  be  wlemn  over  mnstofd  and  pnlpnble  tbmmbosla  of  inttrnul  jui:ulnr  viin  in  uppi-r  part  of  neck. 


DtAONOSIS 

I  CvuiprL-Miion  1043 

Occbml  ComprciuioH  1043 

("■ntusioii  niid  hemorrhngt')  ■ 

s  ThromliOBla.    fimO).  1044 


liich  mny  be  cloudy,  give  globulin  "n<l  ii 

lud   by  loi'til  symptxras  of  piiriilyflin  iiiiil   ■■piisiii. 


■nsod  ci'llular  elements  in  it.    Symptoms  of  CPrebral 
Vini:  w'nb   til.'  locntion  of  the  inflnmnialioo.     Rn- 


Itetnictii>n  of  neck  and  oplstbotonoti.     revcr.  hrndadic,  delirium.     ConvnIiioiiB  and  reirnction  of  nMnmon.     Paralysis  of  cranial  nerves.     ICemig's  sign,     Lumbar  puncture  and  examination  of  the  fluid, 
Irritation  followed  by  those  of  paralysis.     Pulse  usually  small,  irreg^lcir  md  rapid,  except  in  terminal  stage  when  it  may  be  slow.     Optic  neuritis  i>  riir.'ly  present. 

An  acute  disease  chnraeHrlKed  by  prmcrat  symptoms ;  anch  as  fever  with  sloir  pulse,  bcndache  and  vomiting,  convulsions  (especially  In  children),  m-ntnl  confusion,  delinuni,  drowim-s*  and 
I      cephalitis  bns  been  aubdlvided  Into  n  number  of  special  forms  ot  dlse:iw«  detcrihe>l  •■ls<-whcre  in  these  ch^irts.    See  40ii   (encephalitic  fonn),r>42.  ri43.  CM.  1047.  104S. 

The  dl'ease  often  folliiws  no  attack  of  influenza,  and  is  of  acute  or  sub-ncmi-  onset     Hii  mr.sc  striking  feature  Is  profound  somnolence,  from  which  the  patient,  williout  much  dillicuJty.  can  be  an)U5>>d  to  fairly  cliNir  coneciousix'vs.  tempomrily.    With  this  snini-eomn  lire  nssociatetl  a  pHmlyais  ot  one  or 
"j      mow  of  the  mot-T  cranial  nuclei,  especially  of  the  motor  nculi,  and  a  i>rolaund  vfivil.Ti"=i,     The  sensory  cranial  nuclei    are  not  affected.     There  is  no  pnnilyxis  <it  the  eslremities  or  alteration  of  their  rellexes.  oic«pt  very  nu-.'ly.     There  i«  lililc.  m  no,  disturbance  of  the  intellect,  except  In  the 
psychotic  form  (delirium).     No  pain.     .Moderate  fever.     The  blond  is  notusl.  but  thf  .■■■rebrd.Bpiniil  fluid,  almost  always,  shows  a  moderate  lymidioeytosis.  ami  a  definite  increase  in  globulin.     In  addition  to  the  lethargy,  some  wises  exhibit  cataleptic  symptoms:    while  others  sliow  well  marked 
I      syniptonks  of  paralysis  agitnns.     The  mortality  from  the  disease  is  biRJi,  and  the  r^sintial  cause  seems  to  be  n  hemorrhagic  iuflammation  of  the  Drain  stem,  attacking  uspeoially  the  motor  nuclei. 


Menlncitm.    (tiPO.   1108). 

I'Trn-ephalitia. 

(405.  .-VIS.  MH.  5-11.  1047.  104.<!). 

Kiiiilemic  Ehicephalllis. 
Bncephalitis  (.ethargica,  (tJOO,  UIO,  i'>771. 


No  preceding 
injury  or  disuse. 


History  of  a  previous  lilneas.  of  which 
(he  coma  is  only  one  symptom,  and  often 
the  Icrminai  one ;  or  the  prcaenee  of  an 
Inflammation  of  the  scalp  (erysipelas, 
-m.purritloul.  or  of  the  bones  of  the 
kull  f.^ries  and  especially  suppuration 
II  llie  hones  of  the  ear). 


niatory     or    other 

idcnce  of  poison-     | 
log.  I 

.  Convulsions  absent. 


ICvidcnce  of  a  .Hr-      Often  a  slight 

inad»iuacy.  npasm    or    riiddily 

during  the  attack. 


After  UDCerinin  prodromata,  coma  and  paralysis  with  fever  appear  and  death  r«<ull*  >n  two  or  three  weeks.     The  diaeaae  uau&lly  occurs  in  young  persons  and  seems  to  be  due  to  poisoning,  especially  alcoholic.   Optic 
r     polioencephalitia  superior  hemorrhagica  acuta)   or  may  he  in  the  form  of  a  hcmipl''^in.  partial  or  complete. 


turitis  may  be  pri'si 


TIic  p;>rilysiB  may  attack  the  eye  muscle*    (Wernicke's      A.m.-    Multiple   KnivphaliUs.    (496,  643^).     I'M^ 


Headache,  vertigo  and  romitinv.    Often  mild  delirium.    A  recent,  infected  wound  orotln' 
general  and  reseralile  those  of  a  rapidly  growing  ;umor.    Choked  disc  occunrathw  mi 

Headache,  vertigo  and  vomiting.    May  be  a  history  of  former  injury.  No  (evsr.    Ocmi-^e 
tumors  at  the  base  are  more  likely  to  cause  paralysis  of  one  or  more  ■  mtinl  nen  -. 

Memtplegia  or  diplegia  ocriirrioe  in  early  infancy  is  common.     .\  motor  monopl^a   ' 
feet.     Itpileptiromi  convultinns,  unilateral  or  bilateral,  are  frequent.    HemtntheliK 


iiisp.  or  origin,  for  snppura 
The  general  symptoms  ai 


Moderate,  irregular,  often  absent,  fever.     Course  is  progressive  but  may  be  very  acute  or  eitrcmely  chronic  and  often  almwB  a  latent  period.    Tin;  symptoms  are  both  local  ai 
re  prominent  than  the  local.    Suppuration  of  the  middle  ear  and  of  the  mastoid  cells  must  be  carefully  e.tcluded.  especially  in  oltildrcn  (see  50S1,    Pulse  usually  regular  and  full. 


Mental  deterioration,  but  local  symptoms  are  often  as  prominent  as  the  general,    Convulsions,  especially  Jacksoninn  epilepsy,  are  common,  f 
s  very  common   (see  .107.  S071.  especially  when  the  tumor  is  situated  in  the  posterior  fossa  of  the  skull. 


larthria,  etc.)   is  rare.     Usually  some  arrest  of  development  of  the  paralysed  part  and  of  the  sliull.    Little  or  no  niusculm 
and  hemichorea  freaaently  complicate  the  disease  and  cnntractuii's  occur  In  nimofct  every  case. 


rophy,  and  refl-xe* 


liecially  ivhen  tumor  ta  in  or  near  the  CFirtei;    while 
Ankle-clnau*  and  Unblnski.     Tsunlly  tome  mpiital  de- 


IVoBr^Birive  mi-ntal   impairment,  childtsbness.    restlcMness,   amiable   hut  irrilabK  Stendily  increasing  di-mentia.     Blurted   speech.     Tremor  of  lipa.  tongue  and  hnnda.    Tenninnl  dementia.     Inability  to  repent  diflirult  phraaea,  due  partly  to  parnphaKln,  partly  to  loss  of  memory.     Wriline  imperfect : 
wobK  ayllablea  and  letter«  are  left  out  and  letters  doubled.     Apopleciitonn  and  .'orniilslve  attacks.     Ahnormntitics  of  pupil.     Areyll-Robertson'a  reflex.     Lumbar  puncture  gives  globulin  and  lymphocytosis  in  cen^ro -spinal  fluid,     iliitory  of  syphili*.    ro.«itivc  Wassermnnn  reaction. 

Ilislorj-  of  lead  poisoning,  of  lead  colic,  of  wrist-ilrop.  rtc.     Blue  line  on  ::UDs.    OanvnUions.     Lead  can  be  found  !n  the  urine,  especially  after  the  .idminislration  of  K.  I. 

Intention  tr#mot.    Scanning  dpeedi.    Many  motor  and  ncnsory  symptoms.     SMgeoroted  reflexes.     Ataxia,     Nystagmus,    The  convulsive  attacks  may  he  epileptiform,  npoplcctiforru  or  myol-nlc.    Headache,  ivunpulsory  acta  and  slight  dementia  arc  not  uncommon  symptonis. 

Ilendaehe,  increnBimr  fever,   potyclandulnr  enlargement,  difficulty  In   walk  ind  epecch,  lethargy,  increasing  dmwsinoes.  passing  into  coma  and  death.  Trypanosomes  arc  found  in  blood,  cercbro-flnld  and  irlanda.    Disease  Is  almost  invariably  ronfim-d  to  Nrgrom  and  Is  due  to  the  bite  of  the  TNoslse 
fly  liy  which  to'panosomea  enter  the  blootl  and  multiply  there  during  yean  before  symptonis  of  the  disease  manifest  thnmselves.     At  the  autopsy  a  nieniiiiio-enceiihiLlo.myelitls  is  found. 

Often  tremor  or  twitching,     nistory  or  evidence 


'■.-r-bnil   Absi-ew,  1040 

nr<s.  iM.  r.os.  r.-s.  58".  OOT,  flci), 

rerobrul  Tumor,  (125.  152,  101,  R07,  535-41,     l(fiO 
,-.7S.  rA7.  S30-52-n.02.,Vfl2,  Ofil  I . 

Cerebral  Palsy  of  Childhood.  IWil 

Porencephaly,    {117,  COl.  077,   631.    801, 
10S8). 

Pnresif,    (1106).  1052 

Lead  I'alsy,   (1C9.  404.  584.  TOO).  lOK 

Tiis«eminatcd   Sclerosis.    (060).  10S4 

TiypiinoaomiaaU  or   African    Lethargy,  lO.W 


Patient  can  usually  he  aroused  from  his  wma  sufficently  to  speak  .ind  bis  sptedi  Is  ciriraet eristic  of  intoxicafion :   being  indistinct,  blurred   and  foolish.    Pupils 
of  olcoholii-  alms".     Alcohol  may.  pns<iib!v,  be  found  in  the  urine  by  miring  it  with  a  solution  of  pnlnssiuni  lii-chmmatc  and  underlaying  it  in  n  test  tube  w 


dilated  and  respond  to  light.    Flushed  face  and  conJuncrtTa.  and  steriorous  roHplratio 
«rong  sulphuric  ncid,     A  green  color  indiftites  alcohol. 


Pupils  are  contracted  and  do  not  respond  to  licht.     Pnt 
taken  morphine  or  opium. 

Patient  la  in  n  confined  space  or  room  in  which  there  is 

nk  or  ah«enl   ■ 


?  dull. 


Sudden  nttnck  of  coma  with  palloi 
small,  extremities  cohl.  rcstle^sni 


yawning.     T, 
Sudden  Intenniuion  of  heart  beat  during  a  considerable  fraction  of  a 


dr.'Wff,  and  men 
lellof  illnmloatiiii! 


■diac  action  of  tlarl  dur.iliF>i 
inl  tension,  sleafliiy  BTttwiin; 


■npnble.    RpAplratlon  is  slow  and  stertorous.     Face  is  congested:    skin  cold  and  clammy.    Pulse  is  first  slow,  but  later,  especially  i 


fatal  ( 


.   bcni 


t  rapid,     Flislor 


jvldei, 


•  of  patient's  hai 


:vml  gas.    He  is  cyanotic  with  rapid,  irregular  pulse.    He  often  vomit*  and  exhibit*  r 


Oflel 


pre. 


edcfl  by  tinnihrs  annum,  dimness  of  vision,  cold  sweats,  and  t: 
ir  altacfcx  of  syncope  have  been  described  as  occurring,  very  m 


M«ca,    Slinht  Hpnsm  orrlgidity  Is  freqin 
ly.  in  Raynaud's  Dlaeiisc. 


clonic  spasm, 

t  durinc 


e  attack,     in  intermil  hen 


,■  the  onset  of  the  coma  Is  more  t^adunt,     I'uNe  Is 


linolt  or  meri' 


Sudden  attack  of 
coma  ot  short  du- 
ration with  or 
without  n  convul- 
sion. Tlnually  a 
history  of  similar 
attacks  and  often 
of  remote  injury. 


Convulsions  almost 
nlways  present  and 
are  usually  the 
most  striking 
aymiitom  ot  the 
disease,   but   not   so 
chamcteristic   as 
umvnseiousness, 
which    is    at    times 
the   only   symptom 
of  the  attack. 


lower. 

iviih  coma  and  slielit  spasm.    Slow  pulse,  atheromatous  nrleres.    tlaunll.v  occurs  in  ndvancml  ngc. 

miulsicn  lasts  only  two  or  three  minutes  and  is  nccnmpanied  iind  followed  by  a  conin  which  cmdually  pas-scs  into  n  itei-p.  This  post-opllentic  cniuii  is  S'uneiimes  iit'irnt  and  is  sonn-time*  replaced  by  unconscious  ac- 
en  iitncfc  of  ceni'riil  oinvulsions  Is  called  "the  major  attack"  or  "le  grand  mil."  At  iiuie*  such  an  alL-ick  follow*  nu'itlier  immedintely  lliponghout  a  |..ue  series  fsialii-*  epilcptl.-usl.  Al  other  times  there  Is  only 
(,.u  ;  uncimmou  nii^vements  of  lips  nnd  jaws  beins  cmmcn.  This  is  cnllwl  "the  minor  nttnck"  or  "le  petit  nml."  R<miPtlmes  the  nttack*  occur  i-nlr  at  iiiaht  (unctumnl  epilepty).  At  limes  an  attack  of  insanity 
-  tiniSlir  to  the  post-epileptic  insanity.  Tliesc  attacks  may  la*t  minute*,  hour*,  nr  da>-s.  and  in  tliem  the  patients  le«e  their  foraaer  Indivlluallty.  In  sonic  of  tbc^e  attacks  (ambulatory  automatismi  the  patients 
.•r  .ill  iillnik..  there  is  amne-in.  A  rare  form  of  epilepsy  is  one  in  wiiieh  llie  pnllent  falls  suddenly  to  the  ground  and  get*  up  again  !mm'd=nie!y  wttltiiu!  anv  »ppr.>ciil>te  lo»«  of  eonscioosnesa  fvertiirinousl.  The 
mxciou^nesj  diirinz  it  nnd  the  complete  or  almost  complete  absence  of  any  meuwry  of  it.  In  the  interval  helween  lb-  itttnck«.  which  at  tlm-s  exteniN  on  r  mouths  and  yctrs.  the  patient  may  be  entirely  normal.  Fre- 
rtreme  dementia,  especially  if  ihe  attacks  are  freiruent  and  rest  on  a  strong  lieretlitnry  basis.     This  condition  is  not  to  ba  eonfepHuWI  with  ih.*  transitory  mental  Impairment  due  to  bromide  given  them- 


The  attack  usually  commences  with  a  convulsion,  as  described  in  Chart  X.  575,  "Hie  e 
lion.  sfmellmcTi  iriiinl.  sometimes  a  deed  of  violence  f post-epileptir  in=aiiily).  Such 
uncijn«eioii.nes9  and  no  convulsion  and  cither  no  action  or  som..  trivia'  ot  fooliili  net 
reidneei  the  eonviilaive  attack  and  is  called  the  "iisyebic  couivalent"  and  is  altogethe 
wander  about  and  take  joumej-s  and  are  lost  to  iheir  friend«  nnd  to  theBwelveB,  ,\f 
essential  charaet~ri«tic  r,f  tin  epileptic  attack  is  ihe  complete  or  almost  woiplete  unc 
luenlly  he  is  irrJlahle  nnd  shows  some  mental  weakness  which  may  slowly  im-renie 
peuticnlly.    On  the  other  hand,  many  epileptics  have  attacks  during  raanj  years  and  yet  shinv  little,  or  no,  mental  impairment.     I^pilepsy  beginning  in  a  patient  over  forty  .v 


s  of  tir-  should  sugci'st  the  possibility  of  a  corehral  tumor. 


Sudden  attack  of 
unilateral  paraly- 
sis. Rarely  the  pn- 
j  rnlysia  comes  on 
I  slowly.  stMdily  in- 
j  creasing  during 
I  honra  or  days : 
TngmTesceDl  apo- 
plexy." In  tuch 
s  Ihe  c 


Albumen  and  cflzta, 
or  sugar,  or  all 
three.  In  urine. 


(Convulsions  arc 
rare,  but  both  tonic 
and  clonic  spasms 
may  o(vur.  in  vol  v- 
ini;  one-half  of  the 
h<'dy  when  the 
lef.if.u  is  cortical. 
or  involving  hot* 
Bide,  of  the  body 
when  the  hemor- 
rlin;:e  oecurs  In  the 
bruin  stem  (4ti0) 
or  ruptures  into  a 
ventride. 
No  convulsions. 

Convulsions  usu- 
ally. 


I  The  alt'H'k  is  nlloncther  similar  to  the  major  attack  nf  epi|pp«,v.  but  it  does  not  n-ctit.   Tl 
distendrd  abdomen,  fi.ul  smelling  feces,  vomltinc.  diarrhoea,  etc..  and  ceiwt  wheo  llic 
Sudden  attack  of  tickling  end  burning  in  larynx,  suffocation  nnd  striduloiB  bmotbing.  falling  to  the  ground  unconacious  for  a  taw  minutei 


I  usually  be  r-fcrred  to  a 
A  rare  form  of  tabetic  crisis  {Iaryni:enl  i 


The  coma  comes  on  instantly  or  in  the  course  of  n  f(,w  hourii.  There  arc  >tertOTOiiR 
flaccid  paralysis  in  tlje  form  of  bemlplogio.  The  hilaiernlly  inmrvateil  muiclw  [upp, 
lar.vnEcal,  respiratnr.v.  nhdominal.  micturition,  defefralion.  ctc.t  .>8cnpe  peniLanrat 
ent  from  Ihe  start.  The  other  reflexes  may.  durinc  the  coma,  b-  nbollshfl.  Ut^  1.1 
may  die  In  coma  or  the  coma  may  pass  awny  after  sevi-rnl  ho  11*  or  days.  The  low 
paralysed.  Tontue  protruded  towards  the  paralysed  side.  Usually  there  Is  alsn  ni 
diinpneaw.  hut  which  may  be  permnnent,  in  whieh  latter  e«*e  the  mntnr  paraljiis 
Iinpmv.-m-nt  uMially  besins  in  flie  face,  next  in  lea  and  finally  In  llie  arm.  !„  en,, 
tMeiiires  appear  In  aim  and  extensor  contracture  in  leg.  Pr.*!  hemipleiric  motor 
band.  Some  mental  impairment  persists.  I-ocal  sj'mptoms  sneh  as  aphasia  may  or 
lesion  may  cause  an  exacerbation  ot  the  symptoms  In  the  sccmd  week.    RepeAtsd  a 


ronvulsioM". 


inri  of  the  huily  or  10 


iiiUy  ,Ti. 


•|.\v    (Itill 


4<nd  t  il.-r 


n  disc 


'oclnted  with  digestive  disturbance*. 


nemiplesla  disappears  nulcklv 


rcipirniion    nnd   a   slow   pulse.     TTsually  ^Pr<slromiil  H.vmptoms    (hi-adarhi 

n  facial,  ocular,  masticatory,  deglutition.  1      and  ci'mplrtcly. 

^r™!e;i    ^Ro!enhach^^^^^"pa^n;       1'r.slromal  »ym,.t..ns  may  or  may  not  be  present.     Profound  and  ion.  cou,a  u.unlly.  Hk-h  nrlrrial  le,„i.,a    (ns,„,-lal..l  with  cerebml  miliary  aneuri- 
er  hnnch  onlv  of  the  facial  Is  decldediv  '"'"^  cimtSnuid  hemiplesin.     Aire<l  patient.     Presence  of  interstitial  nephritis.     Iramedlale  cjiusc  may  be  exertion   (stiMtnlni;  at  stool)  or  excitement. 

fir«t  a  sensory  hemipleiiia  which  fiuiekly  \  j;„  prndromatii.    Youthful  patient,    rnnliac  or  pulmonary  disease,  sepsis  or  nncurisfli.     I'-tistcuce  of  embolism  cls-where  In  holy.     SHeht  or  absent  cfirna.     Pntae  not 

tly  improves  or  entirety  disappears,  j      ,!„„.      Il,.fni|',|.-.;in  uor  so  permnnent.     Paralms  of  some  cortical  function:  aphasia,  hcmiannpin.  etc.     Spiismt  not  infreoucnt. 

pha.via,  hemlanopin.  etc.    A  mild 


Alhemmnloiis  arteries  or  history    "f  ■yidillis.     Paralysis  of  wme  cortical  function  : 


Omvulsio 
•luently. 


Patient  emaciati-d.     Acetone  odor  of  hn-ath.     Pulse  Is  small  and  rapid.  sKio  ^ry,    Rri,, 

Oniet  usually  gradual.    Som*  edema,  cyanosis,  restlessness,  rnpld,  noisy  respiratinn. 
tains  albumen  and  cniiis. 

Oecurs  at  the  oixet  of  acute  infections,  cspeclntly  In  children.     Often  B»*wi>t#d  »||), 
J      of  this  nature.  Imi  in  these  ease,  convulsions  are  Tare,  and  the  cause  may  eonilst  In 

History  or  evidence  of  expomire  to  itreat  heat.    Absence  of  pereplratlon.    Thecoma  co 
I      lymptoms  (paralytic)  occarionnlly  oecur. 


labored  nnd  may  show  "air  hunger."     Sugar  and  almost  always  albumen  iind  Cfists  also  in  nnne. 
Pulse  ot  high  tension.     History  usually  ot  headache.  TOmtdng.  dyspnoea  and  dimness  of  vision.  Ophthalmoscopi 


acute  Indigestion  with  foul  smollinc  fece=.     Hish  fever  is  common.     Often  history  of  improper  food.     The 
a  failing  cirnilatlou  (cerebral  anemia). 

mi's  on  rapidly  but  not  instantaneously  and  Is  preci-ded  by  many  prodromata: 


\f  bIi'iw  albuminuric  retinitiii.     In  nirc  ciises  there  may  be  bemipleein  or  other  paralysis.     Urine  con- 

■hich  occnrs  in  the  course  of,  and  especially  towards  Ihe  end  of  acute  Infectious  fevers  Is  probably 

headache,  mental  confusion,  mnrkcd  disturbance  ot  i-ixion.  parvnthesiae.  weaknces.  etc.     Delirium  In  a  common  symptom.   Local 


ecping  Sickness. 
Aleoliolic  Coma.    ("tl7l 

NiLre.itiKm    ftnm   opium,   etc.    (054). 

Illuminating  or  coal  gaa  poisoning. 
Syncope.     Internal  Hemorrhage. 

Sii>)(es-.\dams'  Diseaae.    (426,  5S!). 

l-:pilep«y.    (111-27.  420,  575,  849. 
miiv  73  W,  111*4). 


HBO 
1057 
IfttS 

lino 

I0(»i 


flexor  con-  1 

ly    ocfur.    especially    in  Prodromal  *yni|>lonis  present.    Rllgbt  c --     -- .,,  .  ... 

eur.     A  reactive  inflammation  about  the  trausilnry  f..rni.  with  tendency  to  relapses  and  without  contracture,  is  Ibc  so-ealled     lacunar  hcmipl(«sia."  in  which  not  one  large  focus,  but  numerous  minute  toci  ot 

Hacks  at  varying  Intervals  nre  common.  1      softenine  occur  in  the  cortical  nre.i  involved. 


l-:.larop«a,   (57rt).  1002 

Tabes,    (001)-      Uryogeal  cris**).  lOflEi 

Pn<'liyiueningitis      Internn       llemorrhaKiert  I'll!'l 

(502.  588). 

Ceriibral  Hemorrhage.  "^M 

(1+7.  405-0.  noi,  r.<w.  sin-co-i,  imsm). 

('crebral  Knd.oliina.  (005.  836).  H"-'' 

(■,r.l.riil  Tbromlxwis,    (506.  832,  J207I.  lOOIJ 


Diabetic    Oima.  'Wi 

llreniie  Coma.  (678,  Sffl,  «3,  05T).  1068 

Toxic  or  Auto-'l'oxlc  Coma.    (006).  1000 

Sun-lP.kv  or  Ini->lairon,   (n«fl.  (HW).  lOTO 


CHART  XVIb 

Pseudo-coma,  Double  Personality  and 
Weakened  Mentality 


Comprising  Numbers  1038  to  1040  on  left  side  of  Chart 
and  1071  to  1077  on  right  margin 


199 


DIAGNOSTIC    SYMPTOMS    AND    TESTS 


1038 
rSEUDO-OOMA. 


UODBLE  PERSONALITY 
AND  AUTOMATISM  (209). 


Hysterical  symp- 
toms   (415). 


Hysterical  symp- 
toms  (415). 


Epileptic   symp- 
toms  (575). 


Convulsions  and 
Spasms   frequent. 


Convulsions 
frequent. 


IMO 

WEAKENED  MENTALITY. 
Patients  appear  to  be  intelli- 
!;ent,  but  incapable  of  Ions 
sustained  effort,  and  of  self- 
i-ontrol,  often  foolisb  and  un- 
reasonable. The  different  dis- 
eases in  these  groups  merge 
into  each  other  and  no  sharp 
line  can  be  drawn  between 
them.  They  all  rest  on  a  neu- 
rasthenic basis,  and  in  all 
suggestion  plays  a  great  part. 


.\ppreheiLsion     and    various 
prominent    symptoms.      In 


phobias    are 
consequence 


of  their  weakenixl  mentality,  these 
patients  cannot  rid  themselves,  by  rea- 
soning, of  their  uureasonable 
bensions  and  fears. 


appro- 


DIAGNOSTIC   ANALYSIS   OF  S 
PSEUDO-COMA,    DOUBLE    PERSONALITY,    AND 

These  diseases  merge  into  eadi  other  and  into  iusai 
cases  occur  and  in  all  suggestion  (auto-  and  foi 

ABSTRACT   OP   SYMPTO 

Occurs  usually  in  girls  and  women  of  an  emotional  nature, 
be  stopped  by  a  strong  and  continued  pressure  on  ovaries 
tion  will  usually  show  that  she  is  attentive  to  her  surroui 
from  external  causes,   or  auto-suggestion    (hypnotism,  so 

•Patient  seems  at  times  to  be  in  a  hypnotic  state,  or  in  an  a' 
and  in  that  state  to  lead  a  life  carried  on  from  former  sin 
states  from  auto-suggestion,  patients  often  act  like  autom 
ception  and  in  some  hysterical  patients  may  well  be  due  1 

While  in  an  unconscious  state  patient  often  performs  compli 
has  no  memory.  Whether  in  such  unconscious  state  he  ca 
doubtful.     While  unconscious,  epileptics  often  perform  at 

The  symptoms  are  tho.se  of  a  general  exhaustion  of  the  nerv 
bility,  especially  of  the  lower  centers.  It  is  common  in  i 
or  tire  easily.  Every  task  looms  as  a  mountain  before  t! 
ory  and  will  power  are  both  poor.  They  feel  nervous,  irri 
(agoraphobia,  claustrophobia,  mysophobia,  etc.).  Almost 
lack  of  will  power.  The  patient  also  suffers  much  from  p 
ralgias  and  digestive  disturbances.  The  essential  symptc 
is  employed  to  designate  the  most  intense  degree  of  neur 
perative  ideas  and  acts. 

The  patient,  usually  a  male,  is  in  a  condition  of  extreme  ne 
consciousness  in  which  the  attention  is  firmly  and  perman 
pressed  because  of  a  delusion  in  regard  to  a  supposed  disi 
delusion  has  its  origin  in  abnormal  sensations.  On  medi 
idea,  but  the  false  idea  cannot  be  dispelled  from  the  patie 
strous,  fantastic  and  impossible.  At  times  they  seem  like 
and  apprehensive,  and  their  attention  is  firmly  fixed  on  tl 
even  grotesque  delusion  that  some  organ  of  the  body  is  d 

The  di><ease  occurs  almost  exclusively  in  women  and  ehildrs 
system,  are  probably  all  really  cerebral  and  seem  to  be  ii 
adopted  by  the  patient  as  the  result  of  impressions  recei 
patients  are  usually  so  dominated  by  the  desire  to  excite  ■ 
of  accomplishing  this.  Too  much  reliance  cannot,  therefo: 
stimuli  varies  from  day  to  da.v  and  is  often  quite  abnorm 
(416).  Anesthesiae,  parosthei^iae.  hyperesthesiae.  motor 
disturbances  occur  alone  or  combined,  transitory  or  perniE 
often  has  as  its  cause  a  psychic  trauma,  either  acute  or  c 
nervousness,  theatrical  posing,  irritability  and  increased  ! 
ance  of  remarkable  and  startling  symptoms  of  the  greates 
life.  In  general  these  patients  show  lack  of  self-control,  b 
may  .show  wonderful  will  power  or  obstinacy.  Some  of  t 
niata  of  liysteria  :"  others  occur  only  rarely.  The  most  it 
(1(171),  catalepsy  (009),  globus  hystericus  (410),  emoti( 
stricture  of  oesophagus,  torticollis  and  other  spasms  (OIJ 
795),  puralysis  (527),  neuralgic  pains  (051-71),  ovarian 
cough,  dysijuoea,  palpitation,  vomiting,  regurgitation,  an< 
anuria,  polyuria,  melanuria,  hemorrhages,  fever,  flushins 
anosjnia,  ageusia,  concentric  limitation  of  field  of  vision  ( 
tlic  late  "world  war"  a  multitude  of  hysterical  phenomeni 
met  with  and  offered  a  most  interesting  study.  Some  c 
mentioned  in  the  next  paragraph  (traumatic  neuroses), 
from  hysterical  phenomena  long  known  in  civil  life. 

The  disease  occurs  as  the  result  of  traumatism  associated  \ 
iniury.  It  very  rarely  occurs  when  a  severe  physical  inju 
cases  wliere  pecuniai'y  compensation  may  be  obtained  foi 
ceiving  any  compensation.  The  disease  is  closely  allied  t 
scribed  above  under  hysteria.  Tremor,  fibrillary  contract 
paral.vses  (motor  and  sensory),  palpitation  and  vaso-mo 
dreams,  often  about  the  same  subject,  are  common.  Quit 
ing  hours,  and  a  melancholic,  hypochcmdriacal,  mental  st 
of  these  patients  are  seeking  to  recover  damages,  there  is 
tion,  however,  is  far  from  explaining  the  traumatic  neui 
modern  warfare  tliis  disease  is  common  as  the  result  of 
disgust,    fright  and   horror,   together   w-ith   traumatism. 

.\ll  the  vaiious  forms  of  insanity  di'scrilni]  in  thr  n"Xt  chart  e.'chibit,  and  are  in  part  dependent   upon,  a 


.Minormal  and  greatly  increased  suggesti- 
hility  is  the  prominent  symptom. 
Symptoms  are  varying,  inexplicable 
and  incredible.  No  certain  evidence  of 
any  organic  disease;  although  almost 
every  disease  can  be  more  or  less  per- 
fectly simulated.  Malingering,  more  or 
less  conscious,  is  often  present,  render- 
ing diagnosis  more  difficult.  Ovarian 
tendtu'ness  is  an  inii>ort:inl  diagnostic 
symiitivm    (415). 


The  result  of  an  accident. 


IPTOMS 

WEAKENED    MENTALITY 

and  many  transitional, 
i)    is  a  large  factor. 


;Iid-i  are  closed  and  resist  attempts  to  open  tliera.  Coma  can  usually 
2vcn  in  tbe  apparent  coma  the  patient  is  suggestible  and  close  observa- 
gs  and  therefore  not  truly  comatose.  Such  a  condition  may  result 
mbulism.  trance). 

eouditiou  from  auto-  or  foreign  suggestion,  or  from  wilful  deception. 
•  states  quite  distinct  from  the  normal  life.  In  the  hypnotic  or  allied 
[S.  This  is  a  very  rare  condition  and  offers  much  opportunity  for  de- 
aconscious  suggestion  on  the  part  of  the  physician. 

i  acts  and  leads  a  life,  during  hours,  days  or  ■weeks,  of  which  he  later 
■member  what  happened  in  previous  similar  states  is,  to  say  the  least, 
atic  acts. 

systnm,  especially  of  the  brain,  associated  with  an  increased  irrita- 
but  more  so  in  women.  The  patients  are  either  incapable  of  exertion 
so  that  they  are  discouraged  before  they  undertake  it.  Their  mem- 
:,  appi'oliensive  and  have  a  number  of  peculiar  fears ;  phobias — 235 
iarncteristic  of  neurasthenia  as  are  the  phobias,  are  indecision  and 
atii'ii,  vaso-motor  disturbances,  paresthesiae,  headache,  backache,  neu- 
)f  neurasthenia  are  apprehension  and  fear  (phabias).  Psyohasthenia 
jnia  and  exhibits  a  bad  heredity,  morbid  ideas  and  impulses  and  im- 


DIAGNOSIS 

Hysterical  Coma    (1076). 


1071 


Hysterical   .Vutomatism    (]07l>).         1072 


Rpilepsy    (lOGl). 


1073 


Neurasthenia,  Psychasthenia    (114,     1074 
1.3S,    15<V7.    162-4,    lSl-3,    G71, 
074,  S4n-8.  000-70,  1034). 


;heiiia  and  is  greatly  depressed  by  reason  of  an  abnormal  state  of  self- 
'  fixed  upon  the  condition  of  his  body  or  of  his  mind.  Patient  is  de- 
or  abnormality  of  some  organ  of  his  body,  generally  tie  viscera,  which 
•xamination  no  abnormality  can  be  discovered  adequate  to  justify  the 
mi  nd.  These  false  judgments  are  very  various  and  are  often  moD- 
xasgeration  of  the  neurasthenic  phobias.  The  patients  are  anxious 
lis.  The  essential  sy.mptom  of  hypochondriasis  is  a  fixed,  constant, 
ed. 

id  the  symptoms,  which  may  apparently  affect  any  part  of  the  nervouj 
lary;  to  be  the  result  of  a  false  idea  (delusion — 21.5),  or  of  suggestions 
'rom  others  or  from  some  abnormal  sensations  within  the  body.  The 
er  and  admiration  that  they  are  not  very  scrupulous  in  their  means 
!  placed  on  their  statements.    The  reaction  of  the  patients  to  external 

its  results.  The  symptoms  of  the  disease  are  botli  many  and  variable 
ilyses.  convulsions,  spasms,  contractures,  vaso-motor  and  secretory 
,  producing  a  confused  and  constantly  varying  picture  of  disease,  which 
c,  or  more  frequently  both.  In  .addition  to  the  chronic  condition  of 
stibility,  ihe  course  of  the  disease  is  interrupted  by  the  sudden  appear- 
■nsily.  which  render  the  patient  helpless  and  often  apparently  threaten 
the  production  and  maintenance  of  some  prominent  symptom  they 
symptoms  occur  so  frequently  that  they  have  been  called  the  "stig- 
an  I  of  these  acute  hyste'-ical  attacks  are  convulsion  (5S6),  comn 
ittacks  of  laughing  or  crying,  aphonia  (748,  762),  mutism  (747), 
imianesthesia  and  its  transference  (41."),  S37),  astasia,  abasia  (0.52, 
lerness.   photophobia,  tremor    (674),  spinal   irritation,   clavus    (951), 

and  fasting,  tympanites,  phantom  tumor,  false  pregnancy,  peritonitis, 
iating.  angio-neiu'otic  edema  (1201),  blindness  (S55),  deafness  (924), 
,  somnambulism  (1071),  double  consciousness  (1030),  etc.  During 
ill  sorts,  even  the  most  bizarre,  and  of  all  degrees  of  intensity  were 
se  were  associated  with  more  or  less  severe  traumatism  and  are 
rs  were  associated  with  uo  traumatism  and  did  not  differ  materially 


Ilypochondri.'isis    (21G) . 


107 


Hysteria,  Suggestion  Neurosis 
(112-29-31-54-,82,  34o,  415-6, 
r>27.  .586,  018,  620,  064-74. 
747-8.  702,  7*!,  837,  SAO,  Sol, 
870-80,  924.  926,  951,  971, 
KHMl.  1034,  1071-2.  1077). 


1076 


;reat  fright,  or  in  some  accidents  from  fright  alone  without  physical 
a  been  received.  It  is  especially  common  in  railroad  accidents  and  in 
injury;  although  it  occurs  also  in  cases  where  there  is  no  hope  of  re- 
rasthenia  and  hysteria  and  it  may  present  any  of  Uie  symptoms  de 
specially  after  exertion,  vertigo,  parosthesiae,  neuralgic  pains,  local 
isturhances  are  common  symptoms.  Unpleasant,  horrible  and  vivid 
racteristic  of  the  disease  are  insomnia,  especially  in  the  early  morn- 
Most,  if  not  all,  of  these  symptoms  can  be  simulated,  and  as  many 
rally  more  or  less  of  conscious  and  unconscious  simulation.  Simula- 
the  key  to  which  lies  rather  in  "suggestion,"  as  in  hysteria.  In 
ttbiiiation  of  chronic  mental  anxiety,  strain  and  worry  and  of  acute 
as  been  called  "shell  shock" — a  poor  and  inadequate  name  for  it. 

uess  of  the  mental  powers,  varying  In  degree,  but  always  decided. 


Traumatic   Neuroses.     Sometimes 
cnllid  Traumatic  Hysteria 
(1.57,  (11.5.  674.  1034). 


1077 


CHART  XVIc 

Insanity 

Comprising  Numbers  1041  and  1078  to  1082  on  left  side  of  Chart 
and  1083  to  1120  on  right  margin 


201 


y^ 


V 


DUGNOSTJC   SYMPTOMS    AND    TESTS 


DIAGNOSTIC   ANALYSIS    OF   SYMPTOMS 
ABSTRACT   OF    SYMPTOMS 


A  coDditioD  Id  ^icb   (hi-  mind  hna  sot 


fl078 

Amenria  (211). 
Man  or  lew 
eomptete. 
(A  mental  dp- 
fN:t  either  con- 
ireniliil  «t  moii- 
ifonK^  in  in- 
(aneyl- 


dcrtloped  wiUj  nilrancinK 
a  disease  of  tta»  bntio,  cilbi 
or  acquirM  io  iofnocx- 
nif'ntal  defect,  tliesp  pnt 
prpneut  mnuy  find  Tflrio 
'IffecW  nnd  dciormities  »i 
(unnmt  skull,  p'>«l«rior  liy 
hiah  pnlaline  iirth.  coHrsi 
formed  •■nr*.  etc.  The  mni' 
I'lther  ijcncml  or  pnrtinl,  n 
ilB  sliebt  di'sreex  may  bf 
lo  di>foctivi>  tninini;. 


sge,  due  to 
>r  conseoital 
Besides  tlie 
ionis  oftt'D 
u»  plifsienl 
iiph    ai:    de- 

iitin  tnny  be 
diir-  in  nart 


I'liiieiila  aliou  little  vt 
nulk.  U!<uiill>'  :<uil 
iv(juinii£  iuieliigeucG 
outbteak8  ot  anger. 


no  intelJigcoce. 
Uieioseives  witU  u 
and  are  iocapable 
Many  of  tbem  an 


Are  unable  tO!,|)eali  latellieently,  but  ace  often  aoisy.  Many  ace  unable  to 
inoe  and  Ucea,  About  tlmir  unly  dosire  ja  tbal  for  food,  Tliey  can  do  no  act 
of  auataioed  alU'iiiiuii.  .Mum  ot  tliese  [iuii<-uts  L-xtiibit  fr«i)iient  and  violent 
e  uoderaiied. 


AssodatiTJ  nitb  bj-droueplialu6.  There  ia  genecaliy  a  uniform  enlargement  uiib  fontaaelles  and  sutures  unumially  optm  and  btuod.  In  tbe  later 
siBgea  oE  cliroiiic  iiaaea.  tlie  iorcbead  may  be  promineni  (anteriot  born  of  vealmle  tulacseUj,  tbe  oeviput  may  pcuirude  bnclrwac^U  and  tiie  lam- 
bJuid  suture  forui  u  step  ipusteriur  bom  enlarged),  iu  the  milder  forms  ur  iiosierior  bydrocepbalus  the  uieuial  d"teet  may  be  slit^bt,  Brain  often 
sbowK  a  tubecenloiis  sclerusis  witb  nodules. 

Asnuciatisl  witb  epilepsy. 

As^aueialed  wiiti  :i  very  sniull  skull,     lirain  usually  weiglis  less  than  lOUO  eruuimes,  or  33  ouacea. 

Ur.i'un-iu^  iu  family  gcuups,  witb  UHudaess  and  optJc  atrophy  and  u  duck  nil  npo;  in  pla<.'e  of  macula  luccu. 

Aaiueiutetl  witb  congenital  hemiplegia  or  diplegia  and  with  rigidity  ami  cuuvuhions   (5U1). 

AtMuLiatcd  with  no  speeiul  cbaractertjatic. 


ruUenla  cau  talk  and  are  more  or  lew  tkunly  ,u  0,^)^  i,abils.  Tlie>  eiliil 
geiicc.  They  ore  inwipable  of  inueb  edueutiun.  The,  eon  form  (."  abalru 
u  cuiuuiun  and  aesual  insunct  is  ofteu  strongly  dsTeloped. 


DiAQNoeia 

Hydrt)eeplinlic  Idiocy  (11,120).  ■, 


Bpileptic  Idiocy,  II.  101. 
MicrucAphuIli;  Idiocy. 
Amaurotic  Idiiicy, 
r>iri>ucepbttlic  Idiocy. 
Idiopathic  Idtoey. 


Idiocy 
(101. 
743) 


1080 
1080 
1087 
1088 


Leir  ui'lt*  iiu  evident  tliuuijli   low  degree  of  iatelli- 
i;eptiL>jj»  and  uu  bigb   iiiuinl   iikus.      .Masturbation 


I'ulienb)  show  a  degree  of  intelligence  oppr 
eatiou.  even  Uioujiti  m  general  amiable, 
Turtar-like  exprcsaiou  of  the  eouutetiijn 
muy  be  due  in  some  cat>ea  to  poison,  aui. 


>iicliiui;  the  normal  bat  are  evidently  hi'luw  the  Hliitidurd.  when  aubjeeleil  to  tbe  Biuet- 
.'mjuii.'  children  d^'^elup  up  lo  a  certain  puait.  but  theu  litup  aud  uir\er  advance  further 
' .  ^luijting  e^es.  tlileb  Uaaureu  tongue.  auU  ^liort,  atubby  bn^ecs.  I'bey  puaseu  gtea' 
1  ui  vviue  or  tobjcco,    iiuiiple  iutuutili&ui  ia  utten  culled  "uteleiuBis, 


f  Alt  the  clusaca  above  given  under  idiocy  but  witb  Uns  ezttems  'iieniul  defvcLa. 

I  1  ery  delckiive  lulclligeace  in  genera],  but  in  cectum  directions  lusuully  uiu^ic  or  mathematics)  maj  bIiow  great  nkill. 

•{  A^ocJated  with  destruction  or  atrophy  of  the  thyroid  gland.  Arreat  of  gi-uwlb.   Thick,  dry  and  8>.iily  akiu.  Course  feature*  (lllJ4). 

[  Associated  with  no  speual  diacacli!TUitii,'&. 

or  otiier  menial  tests.    They  cannot  be  educated  beyond  u  certain  point.  They  are  ofteu  ohatiDule  and  of  violent  temper  upon  provo- 
.tilismuBj.     In  eouie  cai^es  ol  infant  ill  am  us,  theie  la  a  defective  ^runib  u:  the  body  wiib  ii  i<iiiull  bead  and  a  peculiar  characieriBtiC 
y  iu  imitation    (Kalmuck  idiots  or  muugolismus).     This  J laease  presents  many  ceaemblaucea  to  cretinism    ilUlfJ,  lllM).     lufantilum) 
InfantiliBm  wltu  pcemniuie  seuility  ia  culk>d  "progeria." 


Idiupalhie  Imbecility. 


1000 

Imbecility. 

(101) 


Coctain  feeble-minded  persoDB  seem  incapable  of  uppiefiend'Hg  Uie  aimpleat  iiionil  ideas,  although  their  tueutal  defect  is  not  ao  oix 


i  in  other  directions.     Uu  closer  cKaminatiou,  however,  a  general  mental  defect  becomes  evideni 


1079 

Dementia  (212) 
More  or  Ick 
complete. 
(A  lots  of  men- 
tality, previous- 
ly oequireil.  Srst 
mnntfested  after 
infancy). 


1011  I 


A  condition  In 
which  tbe  mind  bai 
rli>vcloped  to  a  cer- 
tain, even  a  IiIrIi. 
dejtrec  of  intelH- 
gencp  and  then,  in 
conBequenee  of  dis- 
ease of  the  brain 
(functional  or  or- 
fanii'l,  nil  mental 
deri'lopment  haa 
not  only  ceased, 
but  there  liaa  been 
a  diRtinot  retro- 
CfMsIon  which  may 
Ro  on  to  a  com- 
plete Io»»  of  intel- 
Iijri>nce.  Memory. 
rmotioRB  and  In- 
lefi-«t  ore  all  loit. 
Paliput  become 
apathetic,  reacts  to 
no  slim  it  1  n  1 1  o  n . 
•oiN  himself  and 
doM  not  even  cat. 


'  Complete  apathy,  coming  on  more  u 
and  will  respond  to  no  stjmulatio 
i-ellexea  are  exaggeratud.    The  ct 


leas  acutely  ivitb  iiwoui.iia  >ii  the  eaily  muges.  ijui 
•  Appears  lo  he  antsthetic  uiid  .malgeaic.  lialliici 
irsc  ot  tbe  diiictise  U  tniMiupied  at  iluiea  by  pL-riuin 


till  us  aud  deluaious 
\it  tieitement,     Muri 


I'utient  incapable  of  any  mental  ellocl.  Iu  a  dreum-tike  state,  immobile  aud  doi-a  nut  aiiiirvciate  what  i»  guioi;  i 
lire  not  prominent  syuptxma ;  although  the  diaeosc  shows  much  relationship  to  cunfusiouul  miMuity  (llUK).  Tbe  c 
thou  half  of  such  cuaes  n^cui  cr  alter  sevenil  months. 


)        lOM 
The 
I    FeeUft- 
I     Minded 

rat  ImhecllltyorllnbitiinlCriminnlK.  J       <101) 

aiury  IK^nientia  iinil  Stupi.r, 


rariiol  Qpulby.  ratienis  are  dull  and  lUipid  bm  euuclnutaeu  Is  fairly  dear  and  th'-y  uppreiiate  whai 
'm  un  ubacuce  ul  euiotiuus  mid  of  inteicnt  lu  aii.viliitig,  .Vnesthesia  and  analgeaia.  ibey  are  uuwillin; 
They  perform  frcjuently  >.puuirtiieoiis,  impulon.'.  -illy  acts.  They  often  repeat  the  same  act  ur  tbe  i 
vl  u  phrase  which  tliey  have  juai  beard  or  ^pukcu  (eclmlalia),  or  repeat  ubseeoc  wi'i'ds  tcuprulaliu), 
X'he  vncieties  under  tbia  head  merge  into  eacli  ether,  and  all  show,  as  prominent  sjmpcoius,  impulsive 


t  itieni,     llailuciualious  and  delusiuus  are  common.    There 

lit  iiud  uUer  ri>isliinc\.'  when  forced  to  do  it  (negativism). 

lies  istercotjpy).    They  also  often  repeat  the  last  woixl 

bupraiLiaj.  or  remain  iu  any  given  posture  (catalepsy). 

c  pcognoisis 


r  Illsiory  of  alcoholism  and  i 
and  space. 


iated  > 


1   luullilile 


very  i 


ideas  and  a 
re  eases.    A  peculiar  loss  of  memory  with  a  bringing  of  memories  ol  the  ceiuoie  past 


,  at  times  permanent,  often  luiupornry.  com-       Hebephrenic  form. 


:i  Uie 


Hallo. 

lediate  past   (cet 


[vgr.'viive  mentui  deteiioratix 

S  at  puherlj. 

u^    cuuditions   of   stupor   and   exdteiueut,   negativism,   stvreuiypy,    euhololla 

t'uUj  tueutal  deterioration,  at  tim<',s  permanent,  often  temporary. 

iiii'Us  and  partially  syateuiatined  delusiuus  witb  steady  mental  deterioration. 


Usually  ocvur- 

rinp  in  ndult  life 
after  2£i  je^n,  but 
may  occur  in 
youtb. 


I  Occuriing  In 
old  nge. 


Hidiocy  of  alcoholism  extending  ovec  many  yei 
amounts  Qf  alcohol.    The  aymptoms  at  limes 


Tremor.    Dysarthna.    huatt  uf  memory  and  power  of  attention  and  mental  power.    Delusions  are  frequeut.     >>urmul  and  ethical  ideas  blunted.     Irritobb 
mhle  lliu*^-  ol  paresis  illtKi)    (pscudo-puresis),  but  tbe  dementia  is  less  pronouuced,  the  cetcbro-spinal  fluid  is  normal  and  improvement  follows  ab>liii 


History  of  very  u 


epileptic  a 


(Gradual  loa  of  m>'iiiory  and  lUL'utal  power.     .MasturhuLiun  i 


cuuimou.     Usually  stea>lily  progressive  and  iucuruble,  but  this  dementia  may  ( 
iiiipli-te  losa  of  intelligence.    I'utienls  muy  carry  oier  iutu  this  stage  some  traces 


>f  the  e 


Jj,   failure   to  appreciate   the   celaiions  of   time 

ry  susceptible  to  the  eHecls  of  smalt 

n  eliildliood  and  way  be  traualtory,  in  wblcb  cose  It  may  be  cured  by  bromide. 
J  delusions  of  ibo  former  psychosis.    They  usually  sit  motiouIeB* 


amiiesia- 


aeniimenlal  and  often   ' 
ncc  from  alcohol. 


I'aninoid  form. 
Ivorsakow's  PaychosU. 


lOD.^  1099 

.Xdoleaeent     Infinity ;     tbe     ao- 
f-.,ll«l     Dementia     Precox     or  1100 
Mchisophrenia — a  splitting  of  the 
p^che    (terms  of  lery  doubt-  UCri 
fal  value), 

1102 


Ilialory  of  a  previous  psychosis  which  baa  gradually  pasted  into  a  couJitiun  ol  apathy  and  niur.'  oi 
(apaUietic  dementia)   but  some  cases  show  great  restlessDCW    (a^itutitl  dementia^ 

History  of  syphilis.  Lumbar  puncture  shows  flobulin  ud  lymphucyto'ia  in  d-rcbru-spiual  tluid.  Wussermauii  usually  positive.  .Argyll  Huberisoi is  pheut'Uiciiou  and  often  un  ijuul  pupils.  Tremor  of 'Ips,  tuiigia-  aud  bands.  Lose  of  memory,  loss  of  aelf-rcatraiut,  ina- 
bility for  contiounos  menial  concntratioo.  reukles»ooiKjuid  clmuge  in  cfaaructer  are  early  symptoms.  Speech  blurred,  slovenly  aud  tremulous.  Words,  sylbiblcs  and  letten  left  out  iu  speaking  and  in  writing.  I{<-«llcw,  cxclt^le  and  irritable,  with  exaltation  or  at  least 
cheerfulness,  in  spile  ot  the  illuoss  which  patient  roreiyrec  -guuea  us  ccisteat.  liraudiuse  delusions,  silliness  aud  iueonsiateucy  in  sinking  •uuiru^i  wiih  iuonliuate  preteasiou^.  Gradually  increasing  pbyaiuil  ami  eipeciuUy  menial  weakness  up  to  comidete  dementia. 
No  paralysis,  but  much  pai'i-am  and  especially  aprnxia  (231.  'Si>'-).  ty'areli"<^,  inconsidcr.ite,  slovenly  clothi«,  etc.  Apoplectiform  and  epileptiform  aeisurea  are  uaually  present  in  the  coui'se  of  dia  'iL«e.  Incurable,  but  remissions.  Freijueutly  aswciatnl  with  t^>eB, 
more  rarely  witb  various  forms  of  spinal  sclerosis, 

.Associated  with  physical  weakness  and  with  atheromatous  arferies.  The  dementia  varies  from  day  to  day  greatly  iu  degree  aud  may  lead  tbe  patient  to  do  very  foolish  things  (often  erotic),  while  api>ai-eutly  »une.  Loss  of  will  power  (drunkenness).  Depn-ssion  and 
loss  of  memory,  especially  for  recent  events,  with  retentiou  uf  past  uieraoriea.    Dread  of  impending  poverty.    Desire  to  go  home,  imagining  himself  to  be  in  a  strange  place.     Ucstleas  at  night,  ossoci  itcd  with  hallucinations  and  delusions,    .\tiack8  of  excitement. 


Alcoholic  Dementia.  (058,  1100-12). 


ICpilepiir  Dementia,    (375,  10(11). 
Tvrminol  or  Secondary  Dementia. 


low 

Hslluclnatioos  are 
abuodaot  and  doml- 
Dsnt.  Hallueioatory 
Inannitr  (213-71.  or 
I).-lirium. 


1081 

DeluBion»  are  present 
and  dominant.  Delu- 
aionnl  Insanity    (215) 


10S2 

An  eiaggeraled  emo- 
tional state  is  tbe 
dominant  sympt  o  m  . 
Kmotional  Insanity 
(2041. 

The  insanities  of  the 
neuroses  have  been 
considtr^  under  epi- 
lepsy, hysleria  and 
hyporhondriaiis. 


\  t^'iidilioii  in  which  the  pntient  is  constantly 
rr«iTin(!  faUe  perceptWiN  from  his  different 
si-ntw:  either  visual,  auditory,  olfactory, 
gastatory.  tactile  or  painful.  r.i  from  several 
ur  all  combinpil.  Asooeinted  with  this  Is  al- 
ways a  certain  desree  of  impaimieni  of  con- 
arlousness.  whicJi  weakens  his  judgment  and 
does  not  permit  htm  to  dpcide  that  these 
baltudnetions  are  false. 

\  cindition  in  which  ibc  patieui  has  formed  a 
false  juditmenl  about  things  which  concern 
him.  The  basis  of  thcKe  false  judgmenU  ia 
partly  n  congrnitally  defective  brain  and  part- 
ly baltucinations.  AMOclaied  with  these  de- 
lusions there  Is  always  present  n  varyiug  de-. 
Itft'e  of  impairment  ol  intelligetice.  which  pre- 
v.-nis  the  patient  from  recogniKioi:  the  false- 
nens  of  the  delniion  when  cvideuee  is  pre- 
»-nt«i  to  him  which  would  be  ndniiuaic  for  a 
liuniml  man;  although  many  of  these  pa- 
tients lo  their  own  wny  reason  shrewdly. 
These  delusions  lead  to  irrational  eoudurt  on 
till'  part  of  the  patient  which  would  not  be 
inalloiial  were  Uic  delusions  Irue,  \ 


ilieul  is  overwhelmed  by  a  lai-ge  number  of  bn  Unci  nations  and  illusions  which  cunn 
that  of  those  about  liim,  aud  cspi-cially  doubts  their  intentions  towaid  uim.  He  dot 


witb  his  previous  experiences.    He,  rother  slowly,  becomes  cnfused.  frightened  and  timid.     Dols  : 
ich  mlgtii  be  rational  were  his  hallucinations  true.  May  be  the  early  stage  of  other  forma  of  lusauit, 


Utslory  of  alobollaiu. 
dent.    Oreut  frigbl. 


iilions  and  illusious  are  of  all  kiuda  but  are  usually  visual  and  cuneeru  suakes,  spiders  and  uther  small  griitesiine  and  repulsive  uuimals.    Tactile  haltudnaii 
:i  escape  from  bis  enc'ii^es,    I'rvuounced,  continuous  treiuor  and  insomnia.    Diseaee  usually  lasts  liss  tliau  a  week  and  usually  terminates  in  recovery. 


Many  otlier  poisons  besides  alcohol :  cither  exogcnetic,  such  as  belliidouua,  salicylic  add,  etc. ;  or  autugeuelic,  such  as  uremia,  chol.sterin,  plomaims ;  ur  septic,  especially  when  the  potsou  acU  upon  t 
a  mild  hallucinatory  Insouity  or  delirium,  which  may  lait  a  few  hours  or  days  or  may  continue  during  weeks,  months  or  years.    To  this  group  belong  the  "puerperal  i 


ut  appreciate  bis  s 
,    Probably  n  form 

IIS,  shown  by  fumbling  of  the  liugers,  also  t 
.  exhausted  nervous  system  (post-febrile   iua 


ise  commences  with  fever,  beadocbe,  dased  feeling  and  delie 


\  own  identity  and 
«  uBuulIy  very  eri- 
uity),  may  produce 
iteks. 


"arrsis,  (jeneriil  I'ar 
(KV.Hi.  409-l2-ia. 
1-Jlfl.  1230). 


Senile  Dementia. 
roiifiiKional  Iniuinily. 
Delirinm  Tremens   (llWtl2). 


11(M 
HOG 


1107 
llOS 

noo 


,  followed  by  violent  excitement  aud  violent  actions.    Many  hallucinations.     Speech  is  continuous,  violent  and  incoherent.    Disease  usually  terminati.'S  fatally  in  two  or  three  ' 

History  of  alcoholism.     Patient  bos  formed,  on  ll>e  basis  of  ballucinollous,  more  or  less  permanent  delusions,  especially  of  jealouay  aud  persecution.     These  are  often  so  exaggerated  and  monstioun  as  to  be  grotesque.    A  very  common  delusion 

wives  are  unfaithful.    Patients  often  net  violently,    gome  alcubulic  tremor.    Curable,  and  usually  lusts  lesa  than  a  month  after  uleohol  has  been  withheld. 
Patient  has  delusions  upon  which  he  hasce  his  actions.    These  delusions  are  not  associated  with  any  decided  emotional  manifestations  and  are  at  times  permanent,  at  times  changeable;    but  they  arr  nm  rea<iunc<l  upon  shrewdly  and  u  systematic  theory  is  not  built      Simple  Delusional  Insanity. 

upon  ibem.     Curable  in  most  coses. 
Patient  haa  a   number  of  delusions,  on-    f  These  delusions  are  of  a  pleasant  exhilarating  nature  impelling  to  action,  t-  talk  and  incidentally  to  the  disregard  of  the  rights  of  othera.   These  patients  are  usually  violent  and  dongeruua  to  themselves  oud  others. 

systematixcd    or    nearly    ao   but    which 

are  strong  enough  to  influence  his  con-    '  1  liesc  ueiusions  are  ot  a  d.rpreaslve  nature  and  tend  to  inhibition  of  acEiua  aud  apectli,  to  setf-nbascmeni  and  to  self-destruction.    The  patients  sometimes  seem    to  be  in  actual  slup 

duet    and    bearing      Curable    in    n>o»^  merely  profoundly  depressed  vrith  inhibition  of  uU  action    (melancholia  uttcnllal.    At  times  the  intensity  of  their  grief  drives  them  to  frenxy  and  breaks  IbroLigb  their  inhibition 

L      (MP'us  melaoetiolicus).     Oceaaionally  there  is  restlessness    (melancbo 


Aeuie  Delirium.     Toxic.  Sepiic    Febrile  or  Post-     lUO 
febrile  and  Puerperal. 

Delirium  Crave.  Ull 


aglta 


All  these  conditions  seem  to  be  the  direct  result  of  delusions     Jiuch  patients  ore  very  prone  to  s 


1  men  is  that  Uieir 


( mi-lnncholia  cum  stupore)    or 
impels  them  to  deeds  of  violence 


Acute  AleoboHc  Msnii.     Alcoholic  Halludni: 
(n08-9). 


Symptomatic  or  Delusional  Mania. 
.'Symptomatic  or  Delusional  Melancbolin. 


1114 
U18 


Paiieni  has  many  delusions  which  arc  often  the  result  of  ballueinatlons.  They  ore  fit.-d,  pirmanent  oud  are  reasoned  upon.  Newspoper  paragraphs  on  inditFercni  subjects  and  various  drcumstiiiK 
are  wovm  in  with  the  delui-ioos  in  the  attempt  at  an  explanation  of  Uic  curious  things  which  are  buppeuiug  lo  the  patient.  Tiieae  patients  reus  .n  very  cleariy  and  if  their  premises  ore  granted  i' 
tbiw  syslemotlised  and  some  wild  theory  is  evoHeu  to  explam  ti.em.  The  most  triiial  happeuings,  even  in  the  remote  past,  are  fitted  into  Ibis  system  In  the  most  surprising  and  ludicrous  way.  T 
■kuble  person  because  so  many  persona  buff  themselvM  al.xut  his  affairs,  lu  typltal  ,-ases  the  patient  evolves  first  a  delusi'm  of  observation  (all  things,  even  thi-  most  indifferent  and  remoti> 
■  '        -  to  try  hU  character),  and  bnally  a  delusion  of  Enindeiir  (he  mual  have  a  great  destiny  when  ao   many  persons  si-ek  to  injure  bim  or  to  tempt  him.     In  the  latter  ca. 


:x,ii»:Tnttuii  of  tlie  someiimM  natural 
fetliai:  ot  cndnoss  or  discouragement 
wiih  life.  An  lureditary  pnTdUpudiiion 
>■  frenneul. 

-xaL-B'' ration    of    the    autiirnl    fpeling    of 


happening  is  to  injure  bim 


s  in  the  entire  life  of  the  patient  are  more  or  less  distorted  and 
almost  impossible  lo  answer  their  argumeniA,  The  delusions  are 
e  general  rnuh  is  that  the  patient  regnnis  himself  as  a  most  re- 
lave  refcreucf  to  him)  :  neit,  a  delusion  of  persecution  (every 
to  prove  him  unworthy). 


i.y  the  paiirnt  to  explain  the  melancholy;    />;;  "'J^',,;;^  :„); 
very  prone  to  suicide.    Their  circulation  and  their  iW"'y 


eh  there  is  no  discuverable  adeiiiiatc  cause — "a  doud  Bcttic"  •'\'-r  ilie  mind."    A  pewslmlst.     No  hallucinations,  no  delusions,  except  xurb  n« 
tiar>Jonab1e  sin,  etc.    There  is  an  inhibiLioo  of  mental  and  phy^iial  activity.     Patients  withdraw  themselves  aa  much  as  possible  from  tbe  i 


ire  greatly  dlsorderi^I.     f^irable.    The  secondary  form  of  melancholia 

aistie.     They  have  no  hallueiuniioui 
a  severe  form   (frensy).     t'uiable. 
and  melancboUl  «'»''  usually,  but  not  always,  a  eomparotlveiy  normal  period  between  the 


1  joyous  and  exdted  ^o^.^^^.^f  ""»  ,Jj-';overable  ade<iu«io  .au,. 
'  '  --     -1  is  diTiflW  Into  a  mdd  form  (msniaciil  exdtati 


due  lo  delusions,  I 
delusii'OB.     They  a 

The  duration  and  the 


been  d<icribed  under  1115. 
I  impelled  to  constant  apeecb  and  constant  activity. 


'coudnry  to  Uie  deprcMed  fniute  of  mind  and  Invented 
They  ait  quiet  and  are  pirturM  of  woe.     They  are 


Primary  MelaiiehoHa    (Psycbalirla). 


They  are  violent  and  danfi>Toiiii.    Mania  is  often  syrop-       Primary  Mania. 


f  Alterations  at  long  intervnla  ot  mania  and  melancnoi-  "■'•■  u-.m.,,-.  oui  uoi  aiways.  a  eomparotlveiy  normal  period  between  the  i  wo.    The  duration  and  the  intensity  of  tlie  attaeks  and  the  duration  of  tbe  Interval  arc  very  varying. 
,        ,       K  1-  I  Attacks  of  excitement  or  ..f  depression  may  recur  (>"*^'°'  insanity),  or  may  alternate,  after  a  longer  or  shorter  interval  (drcular  insanliyl.     In  suin«  cuseM  tbe  exdted  and  depressed  phases  are  commingled,  or  thr  nlterolions  are  momentary,  giving  a  "mixed  form." 

ano  meianciiolm.        J      Kmepelio  has  incorporated  nil  of  lht*c  forms  under wc  term     manic-depressive  insanity"  but  the  permanence  of  thla  term  isdoubtful.     Ills  classificuUcn  involves  a  recasting  of  the  nomendsture  uf  mental  dlseoBes,  and  It  U  doubtful  If  the  time  Is  yet  ripe  for  nicfa 
I.     an  attempt.  1 


c'irciilnr  Insanity, 

:Mnnii' Depressive   Insanity. 


1118 

ino 


C^ 


CHART  XVII 


Trophic  and  Sympathetic  Disorders 


DIAGNOSTIC  ANALYSIS  OF  SYMPTOMS 
TROPHIC  DISORDERS  AND  DISORDERS  OF  THE  SYMPATHETIC  SYSTEM 


TissxJES  Involved 


1121 

Trophic  Lesions. 


1122 

Disorders  of  the  Sympathetic 
System. 


Symptoms  Aanalysed 

r  1123 
Muscular  Tissue. 

See  Chart  XVIIa. 
1124 
Cutaneous  and  Sub-Cutaneous  Tissue.     See  Chart  XVIIb. 


1125 

Fatty  Tissue. 


1126 

Bone  Tissue. 

1127 

Joint  Disease. 

1128 
I  Other  Trophic  Lesions. 

1129 

Ganglionic  Disorders. 

1130 
.  Vaso-Motor  Disorders. 


See  Chart  XVIIc. 


V  See  Chart  XVIId. 


203 


r 


CHART  XVIIa 

Muscular  Atrophy  and  Hypertrophy 


Comprising  Numbers  1123,  1131  and  1132  on  left  side  of  Chart 
and  1146  to  115S  on  right  margin 


205 


DIAGNOSTIC    SYMPTOMS    AND    TESTS 


DIAGNOSTIC    ANALYSIS    ( 

MUSCULAR   ATROPHY    AND 

ABSTRACT    OF    SYl 


Muscular   atropliy. 

Lesion  in  peri- 
pheral motor 
neurons. 


[1131 
I  ATKOr 


I IV. 


1123 
MUSCULAR 

TISSUE 


Atrophy  is  rela- 
tively rapid  in  on- 
set ami  usually 
great  in  de?ree. 


1132 

iivi'i:i!'ri;iinn 


.\tropby  is  very 
slow  of  onset  ami 
often  slight  in  de- 
gree. 

Increased  or  nor- 
mal strength. 


1  Decreased 
I  strength. 


Muscular  atrophy 
and  hypertrophy 
combined. 

r.esion  in  muscles. 


Lesion  in  central 
motor   neurons. 


No  lesion. 


Lesion    in    muscles. 


Acute    and    sub- 
acute coui-se 
( inflainniMtory 
lesions). 


Chronic   couree 
(degenerative 
lesions) . 


I'aralysis  is  the 
primary  s.vmptoni 
and  atrophy  is 
secondary   to  it. 


.V  trophy  is  tlie  pri- 
mary symptom  and 
the  paralysis   is 
secondary   to,  and 
consequent 
upon,  it. 


Associated  witli  chronic  .ioint  disease,  especially 
he   found. 

-Musflcs  of  face  (Landouzy-Dcjcrine  type),  or  ol 
are  lir.st  affected.  Some  nl^^ch»>  apparently  h 
hypertrophied,  with  increase  of  interstitial  fa 


\'ery  slow  course. 


Paralysis  is  pri- 
mary and  atrophy 
is  secondary. 


Muscular  fibers 
normal.  A  true 
hypertrophy. 


I  The  hyperlniphy  is  the  result 

The  hypertr(i|)hy  is  due  to  mi 
heredity. 


Calf  niiiscles.  infra-spinatus.  deltoid  and  some  oti 
muscles  are  both  weak  and  atrophied.     No  fib 
some  hypertrophied  and  much  interstitial  fat. 
affected. 


SYMPTOMS 
rPERTROPHY 

UMS 


lete  or  par- 
•li-ctri(;ii 
ou   of 
eratiou. 


iiition  of  the 
ical  pxcitabil- 
iit  uo  reaction 
'eneration. 


'ilistory  of  injury,  wound  or  scar. 

Limited  to  distribution  of  one  nerve  (simple  neuritis) 
or  many  nerves  (multiple  neuritis).  Usually  asso- 
ciated with  sensory  symptoms:  pain  and  anesthesia, 
nerve  and  muscle  tenderness. 

(iroups  of  muscles  attacked  not  corresponding  to  the  dis- 
tribution of  an.v  nerve.  No  sensory  symptoms,  except 
some  pain  at  onset  in  back,  joints  and  muscles.  Very 
rarely  nerve  and  muscle  tenderness.  Globulin  and 
lymphocytosis  in  eerebro-spinal   fluid  in  acute  stage. 

Atrophy  affects  either  the  arms  or  the  legs.  Sensory  and 
other  symptoms  of  myelitis  are  present.  Organic  re- 
fle.xes  are  more  or  less  disordered.  Superficial  and 
deep  reflexes  are  abolished  in  the  paralysed  area. 

Atrophy  commences  in  the  small  muscles  of  hands,  or 
muscles  of  shoulder  girdle,  aud  extends  and  is  asso- 
ciated with  fibrillary  contractions.  Mild  spastic  para- 
plegia  (52.5,  SOO)   in  legs. 

.\trophy  affects  the  muscles  of  tongue  and  lips  and  is  as- 
sociated with  fibrillary  contractions.  Mild  spastic  para- 
plegia   (52.0,  SOO)   in  legs. 

Atrophy  affects  the  hands  usually.  Is  associateil  with 
dissociation  of  sensation  aii<l  often  with  ulceration  and 
mutilation. 


DIAGNOSIS 

Injury  of  nerve  (489,  82i). 


1146 


Neuritis    (488-92.  824,  933,  940-9,     1147 
1173).    (Figs.  33,  38.) 


.\cnte  anterior  poliomyelitis 
(495,  791).   (Pigs.  2C-7.) 


flirouie   bulbar    paralysis    (546, 
(K)4).      (Figs.  21-2.) 


Syringomyelia    (553,  693,  S40-2, 
1009,  1170.  1370-2). 


1148 


Myelitis   of   Cervical    or   Lumbar       1149 
Enlargement   (485,  .550). 


Amvotrophic     lateral     sclerosis  1150 

(517-8,  095,  800).    (Figs.  26-7.) 


1   ankylosis.      Many  of  these  cases  are  neuritic.  but  in  some  no  neuritis  can        -Vrthritic  atrophy. 


1151 


1152 


1153 


nlder  girdl"  (Krb's  juvenile  type),  or  of  legs  (pseudo-hypertrophic  form) 
trophied.  Excised  muscle  fibers  show  degeneration  ;  some  atrophied,  a  few 
v'o  fibrillary  contractions. 

itrophy  is  due  The  redexes  are  exaggerated.     Ankle-clonus  and  Babinski 

ly    to    disuse.  are    present    when    legs    are    affected,    unless    prevented 

ectrical    reac-  by  contractures. 
of    degenera- 


Muscular   dystrophies    (477.    787,       1154 
1158). 


A   paralysis   of  long  standing, 
especially  one  from  infancy. 


1155 


nuch  exercise,  and  is  Indicative  of  increased   power.  Strong  man  or  athlete.  1156 

spasm,  occurring  at   the    commencement    of    voluntary    motion.      Strong      Thom.sen's    disease    (611).  1157 


luscles  appear  large,  but  are  weak:  a  false  or  apparent  hypertrophy.  Other 
y  contraction.  Excised  muscle  fibers  show  degeneration:  some  atrophied. 
iv  course.   All  muscles  are  finally  atrophie<l.     Legs  are  early  and  mainly 


rseudo-hypertrophic    paralysis 
(500)    and   the  muscular  dys- 
trophies (1154). 


11.58 


CHART  XVIIb 


Cutaneous  and  Sub-cutaneous  Trophic  Disorders 


roniprising-  Numbers  1124  and  1133  to  1136  on  left  side  of  Chart 
and  1160  to  1173  on  right  margin 


ENDOCRINOPATHIES 

A  number  of  diseases  in  the  following  charts  have  been  ])roved  to  be  due  to  abnormalities 
of   the   internal   secretions  of  certain  ductless  glands. 


livroid  Gland 


Parathyroid  Gland 


^ituitary  Body 


Supra-renal  Capsules 


f  EXCESSIVE  SECRETION 
or 
HYPERTHYROIDISM 

I  DIMINISHED  SECRETION 

[  HYPOTHYROIDISM 

DIMINISHED  SECRETION 

[  EXCESSIVE  SECRETION 
or 
HYPERPITUITARISM 


I  or 

I  HYPOPITUITARISM 

EXCESSIVE  SECRETION 

1  DIMINISHED  SECRETION 


Exophthalmic  Goiter. 


See  1193 


j  In  adult.     Myxoedema 

See  1163 

'i^  Jn  Infant.     Cretinism 

See  1164 

Some  forms  of  Tetany 

See    614 

f  Acromegaly 

See  1183 

1  Gigantism 

See  1183 

1  Dystrophia  Adiposogeni 

talis 

See  1177 

1  Dwarfism 

See  1176 

No  definite  disease,  but  general  increased 

activity  of  bodily  functions. 
Addison's  Disease 


In  addition  to  the  above  there  is  much  evidence  to  show  that  Diabetes  Mellitus 
may  be  due  to  disease  of  the  Islands  of  Langerhans  in  the  pancreas  and  that  sudden 
death  may  result  from  an  enlarged,  persistent  Thymus  gland. 


207 


DIAGNOSTIC    SYMPTOMS    AND    TESTS 


DIAGNOSTIC  ANAI 
CUTANEOUS  AND  SUB-CUTi> 

ABSTRACT    C 


1124 

CUTANEOUS 
AND  SUB- 
CUTANEOITS 
TISSUE 


Aln.pliy 


1134 
Hypertrophy. 


113') 
Eruptions. 


113(J 

I'Iccralions. 


Tlii'  skill  is  iiiuisunll.v  .suii  iitli  ;iiul  lliin.  Tlie  tiugers  become  pointed.  The 
OL't'iirs  iiuite  frequently  in   niTvous  iliseascs,  especially  in   those  in  whi 

The  hair  falls  out,  either  all  over  head,  face  and  body  (as  in  syphilis),  o 
is  not  changed  in  appearance,  .\llied  to  this  condition  is  the  turnin; 
of  severe  pain,  or  psychic  shock,  or  unknown  cause    (loss  of    hair  dye) 

.\trophy  of  the  normal  pigment  of  the  skin;  so  that  patches  of  clear   whi 

sons  of  dark  complexion.     The  edge  of  the  patch  is  more  deeply  pigmcu 

.See  also  facial  hemi-atrophy,  117!). 

f  The  skin   and   mucous   membranes   everywhere   appear   thickened,    as    if    i 
I 


I 


slightly,  on  pressTire.  The  skin  is  sallow,  dry  and  scnly.  Patients 
features  are  enlarged.  Nails,  teeth  and  hair  break  and  fall  out.  The 
and  hoarse.  Response  is  slow  and  iutellectu.ality  very  sluggish  and  at 
atrophied,  or  destroyed,  b,y  disease.  The  disease  may  follow  removal  i 
and  intestitial  nephritis  may  be  present.  Is  more  common  in  women  tl 
time  of  the  climacteric.  When  it  occurs  in  children  th  y  lieconu'  dwarj 
sence  of  the  secretion  of  the  thyroid  gland  and  it  can  be  cur''d  or  ben* 
roid   gland. 

The  skin  is  thickened,  generally  or  locally,  infiltrated,  very  firm  and  ban 
at  their  ends,  and  the  fingers  become  much  shortened  and  abnormally' 
men  and  seems  to  be  allied  to  myxedema.  The  disease  often  couuuenci 
ends  with  an  atrophy  of  the  indurated  patch    (stadium  atrophic  urn).    . 

Clusters  of  vesicles  filled  with  clear  fluid,  each  cluster  upon  a  patch  of  re( 

nerve  roots  and  strictly  limited  to  their  distribution.     The  eruiition  d 

accompanied,  preceded  and  followed  by  .severe  pains  in  the  nerve,  along 

i       for  months  after  the  rash  has  disappeared.     Rarely,  in  severe  cases,   m 

I       Lymphocytosis  has  been  found  in   the  cercbro-spinal  fluid  in  some  caseS. 

In  some  fiu'ms  of  nervous  disease   (especially  in  hysteria)    elevated  patches 
when    the  skin    is   irritated    (urticaria   scripta,    dermographia — 2<X)). 
do  not.    See  also  Angio-Neurotic  F<<lenia   (1201). 

Successive  crops  of  bullae,  which  are  at  first  small  vesicles  and  increase  t 
eral  vesicles  may  coalesce.  There  may  or  may  not  be  fever.  There  i 
tense.     A  very  fatal  disease. 


r  With  much  loss 
■  of  tissue. 


"Ulcerations  larger  and  smaller 
with  sloughing  and  loss  of  pha- 
langes and  even  whole  fingers 
and  toes.  The  whole  process  is 
painless  and  may  in  part  be  the 
result  of  traumatism  in  the  an- 
algesic parts. 


No  spastic  symptom 
tribution  of  one  oi 
tumors  may  occur 
of  leprosy. 

Spastic  symptoms  in 
to  hands  and   am 
tactile  sensibility, 
symptoms. 


With  small  loss 
of  tissue. 
See    also    Ray- 
naud's disease 
(1195). 


Large,  deep,  sloughing  ulcere  commencing  with  redness 
ally  suffering  from  motor  and  sensory  paral.vsis.  an< 
sure    (sacrum,   trochanters,   etc.),   especially  when   tl 

The  ulceration  usually  commences  on  the  ball  of  the  fo( 
extending  deeper,  until  in  many  cases  it  extends  qui 
ulcer  ver.v  rarely  occurs  on  the  hand.  It  usually  com 
forms  a  sinus.  Loss  of  knee-jerk,  Argyll-Robertsoi 
ent  in  the  majority  of  cases,  while  sugar  is  present 

Ulcerations  more  or  less  severe,  the  result  of  slight  tri 
bronzed.    Symptoms  of  neuritis  (933)  are  present. 


IS  OF  SYMPTOMS 

;OUS  TROPHIC  DISORDERS 

SVxMPTOilS  DIAGNOSIS 

Is  arc  excessivrly  curved  and  are  striated.    This  change       Clossy   sk,n. 
the   [I'ripheral   neiuuiib   are   degenerated. 


1160 


ily  in  patdu-s,  usually  on  the  head  and  face.     The  skin       .Mopei-in     (se-iieral   nr  areata  I.  11(11 

lite  of  the  hair  in  patches,  or  universally,  in  cousetjuence 

ppear.      They    are,    of    course,    most    noticeable    in    per-        Vitiligo   and   I.eiieodeima.  1102 

than  the  surrounding  skin. 

rated,    and    do    not    pit,    or   pit    but     ^  Occurring  in  .My.Mdenui.  Iltj3 

!ry  sensitive  to  cold.     The  body  and     j  adults. 

>vements  are  heavy.      Voice   is  slow     j 

«  disordered.     The  thyroid  gland  is 

he    thyroid    gland.      Arteriosclerosis    - 

in  men,  and  frequently  occurs  at  the 

The  cause  of  the  disease  is  the  ab- 

■d  by   the  administration   of  the  thy-        Occurring   in  Cretinism   and    Dwarfs    (1002.   11 77 1.  1104 


children. 

rhe  bones  of  the  phalanges  become  absorbed,  especially      Selenideriiia  ami  Sclerodactyly.  116u 

able.  The  disease  is  more  common  in  women  than  in 
5  a  local  patch  of  edema  (stadium  oedema tosum)  and 
imes  patches  are  pigmented. 

ed  skin;  the  clusters  following  the  course  of  one  or  two       Herpes  Zoster.    Herpetic  Ganglionitis  or  Neuritis.     IKiO 
up  and  disappears  after  a  week  or  two.     It  is  usually  (!)-K)-7s.  12;ij). 

course  of  which  it  is  situated.    The  pain  may  continue 
and  sensory   paralysis  may  be  associated   with   herpes. 

hite  or  red,  appear,  at  times  spontaneously,  and  always      Urticaria    (1201).  1167 

■h    patches    of   urticaria    sometimes    itch    and    sometimes 

ly  size,  api)car  on  the  skin  and  mucous  membranes.     Sev-      Pemphigus.  1168 

ways  some  burning  sensatiim  and  the  pain  nyiy  be  in-  , 

legs.     The  disturbances  are  limited   to  the  area  of  dis-        Leprous  Neuritis.  ll(i!l 

ire  nerves.  All  forms  of  sensibility  are  abolished.  Small 
ng  the  nerve  trunk,  together  with  other  manifestations 

3,  when,  as  is  usual,  the  trophic  disturbances  are  limited       Syriim'(jniyrliM   or  Morvan's  diseise    (.")."p3,  tJ'cK}.  1171.1 

Pain  and   temperature  sense   lost,   with   persistence  of  840-2.  Kmit,  ll."2.  1187).     (Pigs.  2.5-7). 

r  affected  area.     Kyphosis  and  spondylitis  are  common 

the  skin  and  occurring  only  in  bed-ridden  patients  usu-       Bed  Sores.     Decubitus.  1171 

reurring  almost  always  on  parts  subjected  to  much  pres- 
arts  are  not  kept  scrupulously  clean. 

ot  growing  larger  superficially,  but  slowly  and  painlessly       Perforating  Ulcer  of  Tabes  and    (rarelyl    Syringo-     1172 
irough   the  foot   and   appears  on  its  dorsum.      Such   an 
ices  as  a   corn,   which   ulcerates   and    the   pus,   escaping, 
upillary  reHexes  and  other  symptoms  of  tabes  are  pres- 
je  urine  in  a  small  minority. 

atism.     In  cases  of  arsenical  neuritis,  the  skin  is  often       Neuritis    (4SS-02,  824,  940-9,   1147).  ]17ii 


CHART  XVIIc 


Trophic  Disorders  of  Fat,  Bone  and  Joints 

Comprising  Numbers  1125  to  1128  and  1137  to  1141  on  left  side  of  Chart 
and  1174  to  1188  on  right  margin 


209 


DIAGNOSTIC    SYMPTOMS    AND    TESTS 


DIAGNOSTIC    ANALYSIS 
TROPHIC    DISORDERS   OF 

ABSTRACT   OP    SYJ 


112C 

RONR  TISSTTR. 


1127 

JOINT  DISRASE 


1128 

OTHER  TRO- 

I'lIIC  LESIONS. 


fn37 


1125 

FATTY  TISSUE. 


.\trophy. 


1138 
Hypertrophy. 


fll3Sa 
Failure  in 
flevplopinent. 


1139 

Atrophy. 


1140 
Hypertrophy. 


1141. 
Fragility. 


One  of  the 


("iirliest  symptoms  of  diabetes  mellitus  is  an  inability  of  the  body  to  de 
excess  of  fat  had  been  deposited.  Patients  lose  weight  and  if  the  disease  is  lor 
urine  shows  the  constant  presence  of  sugar.     Atrophy  of  fat  and  emaciation  o 

r.arye  and  tender  deposits  of  fat,  in  lumps  or  in  layers,  widely  diffused  over  arms 
Arms  and  legs  painful  and  tender,  especially  in  the  acute  stage  when  the  fat  is 
frequently  m  middle  aged  women   (often  alcoliolie  or  syphilitic). 

Excessive  accumulation  of  fat,  especially  on  buttocks,  pubes  and  breasts.    Deedenc 

Many  cases  occur,  either  congeuitally  or  acquired  in  early  life,  in  which  the  bony 
so  that  the  individuals  remain  throughout  life  of  abnormally  small  stature.  Tin 
^  due  to  atrophy  or  loss  of  function  of  the  pituitary  gland.  Some  of  these  individi 
(simple  dwarfs  or  decidedly  undersized  menl.  while  others  show  many  pliysic 
elsewhere,  under  infantilism  and  mongolism  (lOr*.".),  cretinism  (10!l.'),  IKy.)  an 
dro-dystrophia  fo-talis)  there  is  a  dystrophy  of  the  epiphyseal  cartilases,  in  couse 
in  length  ;  so  that  dwai-fism  results.  The  head  is  relatively  long,  the  bridge  of  t) 
their  proximal  si'gment,  the  hand  is  short,  the  fingers  broad,  of  almost  equal  lem 
pelvis  contracted,  legs  often  bowed  or  knock-kneed  and  joints  ab  normally  lax. 
Adults,  as  well  as  diildren,  not  Infrequently  become  shorter  in  consequence  of  e: 
as  in  rickets,  osteitis  deformans   (11S2),  osteomalacia   (1185),  etc.,  and  in  conse 

(•In  cases  of  extensive  acute  anterior  poliomyelitis  and  of  cerebral  palsy  of  childhoa 
growth  or  very  slow  growth  of  the  part  from  disuse.  * 

One  side  of  the  face  is  much  smaller  than  the  other,  due  to  atrophy  of  all  the  tiss 
and  fat.  The  process  is  usually  progressive.  It  seems  to  be  caused  by  injury,; 
geminal  neuritis.  Dryness,  scaliness  and  loss  of  color  of  the  skin  are  common  "syi 
which  a  small  area  atrophies,  which  atrophy  gradually  extend-^  laterally  over^ 
bones.  The  process  continues  until  the  entire  half  of  the  face  is  atrophied  and,i 
even  to  other  parts  of  the  body.  One  side  of  the  tongue  is  usually  atrophied.  F 
accompanies  the  atrophy. 

'One  side  of  the  face  is  much  larger  than  the  other,  due  to  enlargement  of  all  the  t 
ally  progressive,  and  seems  in  some  cases  to  be  due  to  a  periostitis. 

The  bones  of  the  head  and  face  are  enlarged,  diffusely  or  nodulated .  and  may  cause 
them.  Headache,  neuralgia,  blindness,  deafness  and  facial  paraljsis  are,  thus,  ' 
are  not  enlarge<l.     Forehead  is  bulging  and  head  Is  often  of  great  size. 

Disease  commences  late  in  life  with  slight  pains,  especially  in  legs.      The  bones  of 
jaw  is  not  enlarged.     The  head  enlarges,  the  legs  and  vertebral   column  become  I 
patients  become  shorter  (even  as  much  as  a  foot  or  more)  and  their  walk  is  affe 

Symmetrical  enlargement  of  all  the  tissues,  but  especially  the  bones  of  the  hands  a 
etc.  It  comes  on  gradually,  patient  requiring  larger  and  larger  gloves  and  shoes, 
shouldered"  (kyphosis).  These  changes  are  often  associated  with  bitemporal  he 
head  and  joints  is  a  common  symptom.  The  disease  is  caused  by  hypertrophy  of 
early  lit''-.  Ijcfore  the  epiphyses  are  joined  by  bone  to  shaft,  gigantism  instead   of 

The  hands  aud  feet  are  enlarged,  and  the  fingers  and  toes  "clubbed."  The  bones  of 
.shown  by  the  X-ray.  These  symptoms  are  associated  with  chronic  pulmonary  dise 
symptoms  vnry  greatly  in  degree  and  extent;    the  mildest  form    lieing  "clubbed  : 

In  some  persuiis  the  hones  are  unusually  brittle  and  break  and  bend  upon  the  slight 
bed.  iSomc  of  these  eases  occur  in  old  age  (senility),  others  ocur  in  middle  life 
lime  salts  (osteomalacia),  while  others  occur  in  children.  The  disease  causing  i 
fecta,  osteopsathyrosis,  etc.     In  many  of  these  cases,  the  sclera  show  a  bluish  ting 


.luints  painless,  enlarged,  abnormally  movable, 
especially  hypcrextension,  cartilages  eroded, 
elVusion  of  synovial  fluid,  exostoses  of  bone. 
The  exciting  cause  for  these  changes  is  often 
painless  traumatism,  at  least  in  part. 


.loint      involvement      not      un- 
common.    Usually  in  legs. 

.liiinl   itivoh-ement  rare. 
Usually  in   arms.. 


Knee-jerks  are  abse 
Bladder  symptoms 

Knee-jerks  are  eithei 
the  lesion.  Pains 
painful  and  therm: 


.\trophy  and  .Vtrophy  or  h.vpertrophy  of  different  organs   (mammary  glands,  tongue,  etc.).  or  othf 

Hypertrophy,  frequently  met  with  and  may  be  due  to  disordered  nervous  action,  but   they  are  o 

value. 


SYMPTOMS 
r   AND   BONE 

^OMS 

t  fat  in  the  tissue,  although  previously  often  an 
Dntinued  become  emaciatctl.  Examination  of  the 
:  in  fevers  and  in  many  other  conditions. 


DIAGNOSIS 
Diabetes  Mellitus  (900.  1172). 


J  legs.    Face,  feet  and  hands  not  much  involved.      .Vdiposis  Dolorosa.     Dercum's  Disease   (1012). 
ag  deposited.    Locomotion  impeded.   Occurs  most 


1174 


1175 


f  hair.    Infantile  genitals.    Dwarfism.    Lethargy.. 

niinvcrk  of  the  body  does  not  develop  normally ; 
s  reason  to  believe  that  some  of  these  cases  are 
are  merely  small  but  otherwise  normally  formed 
leformities.  Some  cases  have  been  described 
icrocephaly  (lOSGK  In  Achondroplasia  (cbon- 
iice  of  whidi  the  bones  do  not  increase  normally 
osc  depressed,  the  arms  and  legs  short,  especiall.v 
and  divergent  (trident  shape),  lumbar  lordosis, 
'  mu.soles  are  rather  unusually  well  developed, 
sive  bowing  of  weakened  long  bones  in  the  legs, 
ice  of  curvature  of  the  spine,  as  in  kyphosis,  etc. 

ecurring  in  infancy  there  is  often  an  arrest  of      Disuse   from   Paralysis. 


Dystrophia    Adiposogenitalis.     (1302).  1176 

Adiposogenital,    or    Frohlich's,    Syndrome. 

Dwarfism,   Microsmia,   Nanosmia,   Achondroplasia       1177 
(1(19.  11Ch4). 


1178 


,  even  of  the  bones,  and  especially  of  the  skin 
ction,  or  cold  and  in  some  CEises  is  due  to  a  tri- 
nms.     The  process   commences  in   the  skin,   of 

skin  and  inward  to  the  fat,  muscles  and  even 
rare  eases,  extends  beyond  the  median  line  and 

in  the  trigeminal  nerve  usually  precedes  and 


Facial   Hemiatrophy, 


1179 


es,  especially  of  the  bones.   The  process  is  usu-       Facial  Hemihypertrophy. 

ssure  symptoms  on  the  nerves  running  through      Hyperostosis  Cranii  or  Leontlasis  Ossea. 
mon   symptoms.      Lower   jaw   and   extremities 


1180 
1181 


body  become  enlarged  and  soft,  but  the  lower      Osteitis  Deformans.   Paget's  Disease, 
and  bowed    (spondylitis  and  kyphosis).     The 


1182 


feet,  lower  jaw.  and  sternum,  also  ears,  tongue,       Acromegalv  and  Gigantism, 
'borax  is  much  enlarged  and  patient  is  "round  (1(I9). 

nopia,  followed  at  times  by  blindness.  Pain  in 
;  pituitary  body.  If  the  disease  commences  in 
romegaly  results. 

e  forearms  are  also  often  enlarged,  as  can  be       Hypertrophic  I'lilmonary  Osteoarthropathy, 
of  a  septic  or  tuberculous  nature  usually.  The 
ers." 


1183 


1184 


violence,  even  on  turning  the  patient  over  in      Frairilitas  Ossium.  Osteopsathyrosis.  1185 

ue  to  softening  of  the  bone  and  diminution  of 
as  been  variously  named:  osteogenesis  imper- 
l  color. 

Pains   in   legs.      Ataxia    without   paralysis.       Arthropathy  of  Tabes  (661).   (Charcot's  Disease).     1186 
Argyll-Robertson's  pupillary  reflex.  (Figs.  24-7). 

)sent  or  exaggerated,  according  to  the  seat  of      Syringomjclia    (553.  (iO.S.  1170).    (Figs.  24-7).  11S7 

arms.  Paralysis  of  arms  (slight).  Loss  of 
with  persistence  of  tactile,  sensibility. 

arts  of  body  (hands,  fingers,  etc.),  are  not  in-      Localized    Hypertrophies   and    Atrophies,    symmet-     1188 
jscure  significance  and  are  without  diagnostic  rical  and  asymmetrical. 


CHART  XVIId 
Ganglionic  Disorders,  Vaso-Motor  Disorders 

Comprising  Numbers  1129,  1130  and  1142  to  1145  on  left  side  of  Chart 
and  1191  to  1203  on  right  margin 


211 


DIAGNOSTIC    SYMPTOMS    AXD    TESTS 


DIAGNOSTIC    ANALYSIS 
GANGLIONIC   AND   VASO-MOTOR 

ABSTRACT    OF    SV: 


112!) 
f:A.\OT,IONIC 

rusoiiDKits. 


1 1 :«) 

VASOMOTOR 
DISORDERS. 


1142 
Pnralylic. 


1143 
Irritative. 


f1144 

'  Vascular. 


114-, 

Exiidativp   nr 
I.  Socrctory. 


I'tiisis  of  cyi-lid  (duo  to  paralysis  of  Miiller's  muscle),  although  paticut  cau  rai- 
o£  the  levator  palpi'lirjo  superioris.  Contraction  of  pupil  (mynsis),  which  ( 
briskly  when  eye  i.s  exposed  to  light  and  on  convergence.  Narrowing  of  palpe 
(exophthalmos).  Intra-ocular  tension  diminished.  The  oilio-spiual  reflex  (33 
on  the  affected  side  of  face,  and  also  on  side  of  neck,  or  of  arm  and  thorax  abr 
of  cocaine  in  both  eyes  accentuates  the  symptoms  by  dilating  the  pupil  and  r 
paralysed  one. 

'I'lie  syrjiptonis  are  exactly  opposite  to  those  of  paralysis  of  the  cervical  sympalh 
widening  of  the  paljiebral  fissure  (Stellwag's  sign)  and  delayed  descent  of  up 
sign).     The  Hoston-Kocher's  sign,  an  amplification  of  Graefe's  sign,  may  occur 

Exophthalmo-s,  tachycardia,  goitre,  flushing,  sweating,  tremor,  nervousness,  delayf 
ward  ((iraefe's  sign),  widening  of  the  palpebral  fissure  (Stellwag's  sign),thril 
thyroid.  The  disease  occurs  much  more  frequentl.v  in  women  than  in  men  anil 
disorder  of  the  cervical  sympathetic  ganglia,  yet  it  is  really  due  to  excessive  se 
which  are  the  reverse  of  those  of  myexdema  (11(>3),  can  be  produced  by  the  i 
be  curwl  by  extirpation  of  the  thyroid. 

Paroxysmal  spa.sm  or  congestion  of  the  hroncliioles,  often  reflex  from  nasal  disea 
nervous  temperament  of  most  asthmatics,  together  with  the  very  rapid  onset  ai 
may  be  due  to  a  disturbance  of  the  thoracic  sympathetic.  The  paroxysmal  aft.' 
prolonged  expiratory  murmur,  nnike  the  diagnosis  easy.  Asthma  is  associated 
he  in  part  voluntary,  in  part  reflex;  also  is  usually  associated  with  bronchitis. 

'Paroxysmal  attacks  of  sub.iective  and  objective  coldness  and  pallor  ("dead  linger) 
or  tip  of  nose  or  of  eai-s  or  of  all  together.  These  attacks  may  last  a  few  minu 
lowed  by  an  attack,  in  which  the  same  parts  become  dusky  blue,  or  purplish  bl 
This  is  associated  with  pain.  This  attack  may  pass  off,  after  several  hours,  wi 
tion  of  them,  nuiy  become  gangrenous  and  finally  slough  off.  The  necrosis  dot 
The  disease  is  usually  s.vmmetrical.  It  is  more  common  in  cold  weather  and  is 
b.v  working  with  hands.  Paroxysmal  hemoglobinuria  and  evidence  of  cong&stii 
tacks.    A  hemiplegia  and  in  other  cases  a  coma,  both  transitory,  have  bein  desc 

.Vnalogous  to  Ra.vnaud"s  disease  is  gangrene  of  extremities  occurring  in  many  met 
old  age;  either  without  the  local  syncope  or  local  asphyxia,  or  wilh  only  slight  : 

j  Parox.vsmal  attacks  of  formication,  tingling,  numbness  and  other  parestbesiae  in  fi 

tervals  and  exclusively  in  women.     They  seem  to  he  brought  on    b.v  overwork  ai 

J       diirin;;  the  attack  the  skin  becomes  pale  and  blue.     Similar  symptoms  sometlm 

I  Paroxysms  of  severe  pain  in  one  foot,  rarely  in  both,  rarelj'  in  hands  and  very  ri 

I       increased  b.v  allowing  foot  to  hang  down,  or  by  motion  of  it,  or  by  cold.     The  p; 

re<lne.ss  and  swelling  of  the  whole,  or  part,  of  the  sole  o£  foot.      Usually  attack 

to  a  simple  vaso-motor  neurosis.     Tlic  neuritis,  wdien  present,  is  often  associate 

Occurs  in  middle-aged  or  elderly  persons  and  is  associated  with  arterial  disease, 
short  walk  and  increases  so  that  walking  becomes  impossible.  It  passes  off  aft' 
ing  the  attack  the  feet  are  cold  and  there  is  absent  or  greatly  diminished  piilsa 
Syphilis,  alcohol  and  tobacco  and  injury  seem  to  be  common  causes  of  this  con 
grene  of  the  feel.  The  arms  are  rarely  involved.  The  disease  Seems  to  be  m 
motor  spasm. 

In  many  diseases,  if  lines  or  writing  be  traced  im  the  skin  with  a.    sharp  i)oint, 
change  to  lines  of  bright  redness,  which  persist  for  minutes  or  hours. 

Parox.vsmal  attacks  of  localized  edema  of  subcutaneous  or  submucous  tissue,  ca 
ing  a  few  horn's  or  da.vs.  The  extent  of  the  edema  varies  grcatl.y.  It  may  be  on 
extremity,  or  even  more.  It  may  cause  death  when  occurring  in  the  larynx.  T 
sure.  They  occur  in  hysteria  and  are  usually  associated  with  a  neurasthenic  c 
are  associated  with  s.vmptoms  of  digestive  disorder,  they  are  called  urticaria, 
eases  except  the  itching.    The  disease  often  shows  a  strong  heredity  and  at  time 


Edema  of  the  h'g-s,  unilateral  becoming  bilateral,  bad  heredit.y.     The  edema  may  1 
being  a  s\id<len  demarcation  at  the  level  of  the  joint.     The  edema  may  be  assoi 


Some  casis  present  paroxysmally  or  constantly  a  profuse  sweating,  usually  loca 


SYMPTOMS 
SORDERS 

rOMS 

•elid  pei-fi'dlj-  liy  an  effort  of  will  by  contraction 
not  dilate  when  shaded,  althoviifli  it  contracts 
fissure  Willi  retraction  and  lowerinii  of  eyeball 
s  abolished,  fhishinir  of  skin  and  absence  of  sweat 
he  third  rib.  In  this  condition,  the  instillation 
i;   the   eyelid    in    the   healthy  eye,    but   not   in    the 


DIAGNOSIS 

I'aralysis   (if   t'ervical    Sympathetic. 
Horner's   Syndrome    (4r>."i). 


1101 


Iiilation  of  pupil  (mydriasis),  exophthalmos, 
eyelid  when  eye  is  turned  downward  (Graefe's 
:his  disease  and  in  exophthalmic  s(iitre   (1193). 

!scpnt  of  upper  eyelid  when  e.ve  is  turned  dowu- 
d  systolic  murmur  in  vessels  of  neck  and  over 
ough  many  of  its  symptoms  may  be  referred  to 
on  of  the  thyroid  iiland.  Many  of  its  symptoms, 
nistration  of  thyroid  gland,  and  the  disease  can 


hriliiticm   of  Cervical  SyiU]inlbelic. 


l'".xopliihalniic    Coitre    (UTi'). 


1192 


11!):! 


Freedom   from   symptoms   in    llie   interval.     The       .\s 
ssation  of  the  attack,  indicates  that  the  disease 
of  dyspnoea,   with   the  abundant  dry   rales   and 
strong  contraction  of  the  diaphragm,  which  may 


(r.ic.t. 


ll'.M 


"local  syncope")  and  tingling  of  fingers  or  toes 
ov  hours  and  then  may  pass  off,  or  may  be  fol- 
("local  asj)hyxia  or  cyanosis")  from  congestion, 
bundant  sweating,  or  the  parts,  or  a  small  por- 
it  usually  involve  the  whole  of  the  cyanotic  area, 
f'n  brought  on  by  putting  hands  in  cold  water,  or 
if  other  internal  organs  may  occur  in  some  at- 
d  in  a  few  cases  of  this  disease. 

■s  of  a  family  at  varying  ages  from  childhood  to 
.■ations  of  these  conditions  in  some  of  the  cases. 

■s  and  hiLnils.  The  attacks  occur  at  irregular  in- 
y  having  the  hands  in  cold  water.  In  some  eases 
ccur  in  t:he  early  stages  of  acromegaly   (1183). 

■  in  face,  lasting  a  few  minutes  or  a  few  hours. 
except  in  the  earliest  attacks,  is  accompanied  by 
>n  only,  and  is  generally  due  to  a  neuritis,  rarely 
ith  atheromatous  arteries. 

lainful  cramp  occurs  in  muscles  of  legs  after  a 
short  rest  to  return  if  walking  is  resumed.  Dur- 
in  the  dorsalis  pedis  or  posterior  tibial  artery. 
on.  The  disease  not  infrequently  precedes  gan- 
y   due   to   arteriosclerosis   associated   with    vaso- 


U;lyii:iiiir> 
I  loll  I. 


Disease 


Svmnietrical    (Jangrene 


Hit." 


Family   (iangrene. 


.Vcrnparesthesia. 


Krythrnnielal-ia    nOHH. 


Intrrniiltei'l     Limping    or 
Aiigiiisrlerotic'.M     i"C<) . 


119(1 


1197 


11  OR 


Claudic.'ition.      Dvsbasia      1100 


lines  appear  for  a   few  secomls  white,  but  soon        DernHigr.-ipbia    (o'iti.   IIIIT). 


1200 


ig  localize<l  swellings,  either  white  or  red,  last- 
ilf  inch  in  diameter,  or  may  extend  over  an  entire 
'  swellings  are  not  tender  and  do  not  pit  on  pres- 
tion.  If  the  swellings  are  red  in  color,  itch  and 
sharp  line  can  be  drawn  between  the  two  dis- 
ems  to  be  malarial. 

imited  abo^e  by  the  ankle,  knee  or  groin;    there 
>d  with  pyrexia  or  gastric  disturbance. 

d,  sometimes  general. 


.\ngio-Neurotie    Edem.i    ami    T'rticnrin.       (11071.        1201 
(Juincke's  Diseasi'. 


Milroy's    or    Meig's    Disease.      Trophcsleiua.  1202 

Ilyperhiilrnsis.      Excessive    Sweating.  12(K! 


M 


CHART  XVIII 

Syphilis  of  the  Nervous  System 

Comprising  Numbers  1205  to  1217 


213 


DIAGNOSTIC   ANALYSIS 
SYPHILIS   OF  THE   WEI 


DIAGNOSTIC    SYMPTOMS    AND    TESTS 


1205 

SYnilLIS  OF  THE 

NERVOUS  SYSTEM. 

History  o£  personal,  or  hered- 
itary, syphilis.  Physical  evi- 
dence of  syi)hilis ;  such  as 
Wa.ssermann  reaction,  a 
chancre  or  its  scar,  indura- 
tion, raucous  patches,  a  syphi- 
litic rash  or  its  copper 
colored  scars,  hazy  cornea, 
notche<l  teeth,  furrows  about 
ansle  of  mouth,  saddle  nose, 
ptosis,  iritis,  enlarged  glands, 
periosteal  nodes,  etc. 
(108,  17.-)  to  180). 


Syphilitic  Nervous  Diseases. 

Symptoms  of  syphilis  of  the  ner- 
vous system  are  very  vari- 
able from  day  to  day,  transi- 
tory and  manifold.  They  con- 
sist of  paresis,  rather  than  of 
complete  paralysis.  They 
usually  show  rapid  improve- 
ment under  K.  I.  and  Hg.  or 
Salvarsan.  Nocturnal  head- 
ache is  common,  as  are  also 
the  Argyll-Robertson's  pupil- 
lary reflex,  unequal  pupils 
and  optic  neuritis. 


Ci  rclinil  symptoms. 

Although  these  symptoms  can 
be  divided  into  several,  more 
or  less  well  defined,  groups, 
yet  a  combination  of  several 
or  all  of  the  lesions,  in  vary- 
ing intensity,  is  not  infre- 
quent ;  so  that  a  combination 
o£  the  symptoms  of  several 
or  all  of  the  groups  may  be 
present  in  one  case.  Pure, 
uncomplicated  cases  of  each 
type  are,  however,  commonly 
mot   with. 


Spinal  symptoms. 

(Both    forms   of   spinal    syphilis 
may  occur  together). 


Cerebral  and  spinal  symptoms. 


.Local    peripheral   S3Tnptoms. 


Post-,  or  Meta-,  syphilitic 


ISL-,   ur   lYieia-,   sypniiinc  rl  erehral 

nervous  disease.    A  term  used   J 

very    infre(iuently   of   late.  [ Spinal  sj 


Cerebral  symptoms, 
symptoms. 


I.iUle  01  no  lymphocyti 
cerebro-spinal  fluid  froi 
bar  puncture. 


(ilcibuliu     ami     decided 
ocytosis   is   found   in   c 
spinal     fluid     from     li 
puncture. 


'.No   globulin    and    little 
lymphocytosis   found   ii 
lu'o-spinal    fluid    from    1 
puncture. 


(iliiliuliu     and     decided  1 

ocytosis     found      in  ci 

spinal      fluid      from  1 
puncture. 

•  iliibulin  and  decided  1 
ncytosis  in  cerebro 
fluid. 


Wasscrmann  reaction  ij 
bloofl.  Normal  eerebrol 
fluid. 

Wasscrmann     reaction 

blood,    usually. 
Increased  lymphocytosis  i 

bro-spinal  fluid. 


'   SYMPTOMS 
US  SYSTEM 


ABSTRACT    OP    SYMPTOMS 


Symptoms  of  cerebral  tumor  (507,  536).  Other  syphilitic  symp- 
toms may  he  present.  Rapid  course  with  irregular  remissions 
and  intermissions.  The  symptoms  of  cerebral  compression  are 
much  less  pronounced  than  in  non-syphilitic  tumors.  Very 
amenable  to  anti-syphilitic  treatment. 

Symptoms  of  cerebral  thrombosis  (SOU).  The  attacks  occur  rather 
early  in  adult  life.  There  are  many  prodromata.  Nocturnal 
headache  is  common.  The  paralysis  is  moderate  in  degree,  vari- 
alile  in  intensity  and  often  temporary.  Mental  derangements, 
often  iu  the  form  of  trance-like  slates,  frequently  occur.  Branches 
of  the  basilar  artery  are  involved  most  frequently,  and  the  at- 
tack often  occurs  during  sleep,  or  without  coma  during  the  day. 


Symptoms  of  cortical  irritation 
(Jacksonlan  epilepsy,  local 
headache  and  tenderness)  and 

.  paralysis  of  cortical  functions 
(aphasia,  monoplegia,  etc.). 
Mental  derangement  is  com- 
mon, and  often  takes  the  form 
of  paresis  (pseudo-paresis), 
but  is  amenable  to  anti-syphi- 
litic treatment. 


Symptoms  of  meningitis  (590, 
(KKi),  which  may  be  very 
slight  and  very  variable.  With 
severe  headache  (nocturnal) 
there  may  be  some  nausea 
and  vomiting.  Little  or  no 
elevation  of  temperature  or 
retraction  of  neck.  No  tuber- 
culin reaction  or  evidence  of 
tulierculosis.  This  disease  is 
rare  in  children. 


Xo  symptoms  of  cortical  irrita- 
tion or  paralysis  of  cortical 
functions.  Paralysis  of  cra- 
nial nerves  (especially  the 
oculo-motorius) ,  progressive, 
of  irregular  distribution  and 
in  varying  degree.  Drowsi- 
ness and  stupor  are  common. 


DIAGNOSIS 
Isolated  Cerebral  Gumma. 


1206 


Cerebral      Sy|vhilitic      Kudarterilis      1307 
anil   Tlirnmliosis. 


Syphilitic  Meningitis  of  Convexity     1208 
of  Brain. 


Syphilitic    Meningitis    of    Base    of     1209 
I'.rain.    including    Kahler's    Dis- 
ease   (Multiple  Myeloma). 


Symptoms   of    Brown-Sequani's    paralvsis. 
{r.\2.  50!),  ,S44,  975-81), 


or   later    of    paraplegia       Isolated  Spinal  Gumma. 


1210 


Symptcuus  of  myelnMialacia    (4S5,  olo-l,  .517-8,  550-1). 


Symptoms  of  lateral  sclerosis   (5251.     (Fig.  20.) 

>h-        Symptoms  of  spinal   meningitis,   or  of   pachymeningitis    (551,   605, 

ro-  974.  1005).     Rigidity  of  back.     Girdle  pains  and  r.iidiating  pains, 

par  e.\ai;gerated    rcliexes   in   legs.      Some   of   these   cases   present    the 

symptoms  of  i>ri>gressive  spinal  muscular  atrophy   (548), 

)h-       .V  combiuatioii   of   the  aliove  .symptoms,   noted   under  1208-9-1.3,   in 
lal  very  varying  extent  and  intensity.     .\  clinical  picture  comprising 

cerebral  and   spinal   symptoms  ami   presenting  great  variations, 
which  are  impossible   to  describe  in  a  few  words. 

he       Symptoms  of  neuritis   (4SS-92,  824^,  940-8). 


Spinal   Syphilitic  Endarteritis  and     1211 
Thrombosis. 

Rrb's   Syphilitic  Lateral   Sclerosis.     1212 

Syphilitic  Meningitis  of  Cord  and     1213 
of  Nerve  Roots.     (Meningo-raye- 
litis.   Pacliymeningitis   Cervicalis 
Ilypertropbica.l 


Cerebro^Spinal  Syphilis. 


Syphilitic  Neuritis. 


1214 


1215 


Symptoms  of  general  paresis   (1106). 
Symptoms  of  locomotor  ataxia  (661). 


Paresis.  1216 

Locomotor  Ataxia.     Tabes.  1217 

(Fig.  27.) 


CHART  XIX 

Abnormal  Cerebro-Spinal  Fluid 

Comprising  Numbers  1220  to  1244 


215 


ri22i 

Globulin  test  positive. 
Wiiite  cells  increased. 


1223 
Leucocytosis. 


1224 
Lymphocytosis. 


1220 

ABNORMAL 
CEREBRO- 
SPINAL 
FLUID. 


1222 

Globulin   test  negative. 
(.White  cells  not  increased. 


DIAGNOSTIC   ANALYSIS   OF 
ABNORMAL    CEREBROSPI] 


TESTS 

Weichselbaum's  diploooccus  in- 
tra-cellularis  meningitidis  or 
rarely    Pneumococcus. 

Weichselbaum's  diplococeus, 

Pneumococcus,  Pfeiffer's  ba- 
cillus, Streptococcus,  Staphy- 
lococcus, Typhoid  bacillus  or 
Bacterium   coli,   etc. 

Tubercle  bacillus. 


Tubercle  bacillus. 


AND     DIAGNOS 

Fluid   may  be  clea 
Tension  increase< 


Fluid  usually  cloud 
liisli   tension. 


Fluid    usunlly    clea 
cate     coagulum 
high     tension. 


Wassermann  and  Colloidal  Gold 

reactions  positive. 


Fluid     clear 
bacteria. 


and 


[Wassermann  and  Colloidal  Gold 
reactions   negative. 


Tension     is     usualli 
but  not  very  high 


1225 

No  lymphocytosis. 
No  leucocytosis. 


No   bacteria  and 
Wassermann 
negative. 


Fluid  clear  with   inc 
si  on. 


:oMs 

LUID 

HNS 

udy.       Ocours  iu  fpiiloiii- 


DIAGNOSIS 

Symptoms  of  epidemic  Cerebro-       I'Ipitlemic    Cerebi-o-spinal   Meniu-        12li<i 
spinal  mcniusitis   (591).  sitis. 


mler      Occurs  sporad- 
ically. 


Symptoms       of      sporadic       or      Sijonidic  Piinilcnt  Meningitis, 
purulent    cerebro-spinal    men- 
ingitis  (592). 


1227 


deli- 
nder 


Acute  course. 


[  Chronic  course. 


Symptoms   of   tuberculous  men- 
ingitis   (593). 


Tremor  and  mental      Symptoms  of  Paresis  (1106). 
symptoms. 


Ataxia, 


Symptoms  of  Tabes  (661). 


Symptoms  not  typically  characteristic    of    paresis    or 
tabes,  being  due  to  a  cerebro-spinal   meningitis. 


ased 


teu- 


"Motor  paralysis. 


Herpetic  rash. 


Epidemic. 
High  fever. 


Symptoms     of     acute     anterior 
poliomyelitis   (495).        (Figs. 

26-7). 

Symptoms  of  Encephalitis  Leth- 

argica   (1047). 

S5'mptoms     of     herpes     zoster 
(1166). 

Symptoms  of  Typhus. 


Choked  disc  usually      Symptoms  of  cerebral  or  spinal 
present.  tumor  (507,  57S,  587). 


Cliokcd     disc     may 
be  present. 


■Symptoms  of  cerebral  or  spinal 
abscess  (508,  578,  587). 

Symptoms      of      hydrocephalus 
(405,   905,   961). 


Pain  and  spasm  in  Symptoms  of  decided  spinal  ir- 
ritation, with  slight  or  no 
paralysis    (524). 


back. 
Headache. 
Apoplexy. 

Albumen  and  casts. 
Anemia. 


Symptoms  of  serous  meningitis 
(594). 

Symptoms  of  cerebral  or  spinal 
hemorrhage   (503,  524, 
1063-4). 

Examination  of  tlie  urine  shows 
albumen  and  casts.  Edema, 
headache,  dyspnoea,  etc., 
usually  present. 

Examination  shows  anemia,  pal- 
lor, etc.,  or  acute  infections, 
or  some  similar  conditions. 


Acute,   or  sub-acute  Tnborculous  1228 
Meningitis. 

[Clironic   Tuberculous   Meningitis.  1229 

Paresis.  1230 

Tabes.  1231 

CJerebro-spinal     Syphilis      (1208-9,  1232 

Acute  Anterior  Poliomyelitis.  1233 

Encephalitis  Lethargica.  1234 

Herpes  Zoster.  1235 

Typhus  Fever.  1236 

Tumor.  1237 

.ibscess.  1238 

Hydrocephalus.  1239 

Heniatorrliacliis.  1210 

Serous  Meningitis.  1241 

Hemorrhage.  1242 

Uremia.  1243 

Anemia.  1244 


PART  III 

Localization 

OF 

Lesions  Within  the  Nervous  System 

BY 

A   CONSIDERATION  OF  THE 
PARALYTIC  AND  IRRITATIVE  SYMPTOMS 
RESULTING  FROM  THEM 


217 


CHART  XX 

Spinal  Localization 


A.  According  to  altitude 

Comprising  Numbers  1250  to  1267 
B.  According  to  situation  in  transverse  area 
Comprising  Numbers  1268  to  1279. 


219 


A— TABLE  OF  SYMPTOMS  IN  TRANSVERSE  LESIONS  AT  DIFFERENT  LEVELS 

OF  THE  CORD 

Modified  from  Wichman 


Involved 


Motor  Conditions 


Reflex 
Conditions 


Sensory 
Conditions 


1250 
V 
Sacral 

1251 
IV 
Sacral 


Paralysis  Paresis 


None. 


Coccygeus. 


Actions  lost  or 
impaired 

Elevation  of 
coccyx. 


Absent 


Anal. 


Anesthesia 
In-      with  a  zone  of 

creased  hyperesthesia 
in        surrounding 

partial    it  or  limiting 

lesions    it  above 


Coccygeus.       Levator  ani. 


Sphincter  ani. 
Detrusor  urinae. 
Trans  versus  perinei 
Erector  penis. 


Elevation  of  Erection 

coccyx.  of  penii 

Elevation  of  anus   dimin- 
Sphincter  ani.  ished. 

Ejection  of  urine. 
Vaginal   constriction. 
•3Baq;^jn  joss3jdui03 


None 


None- 


1 

Spliincter  ani 
Levator  ani. 
Detrusor 

.  Rectum. 

1252 

urinae. 

III 

Transversus 

Sacral 

perinaei. 

Erector  penis 

^ 

Compressor 

^  urethrae. 

'  Sphincter  ani 

Pyriformis. 

Levator  ani. 

Obturator   internus. 
Gemellus  superior. 
Gluteus  maximus. 
Biceps  femoris. 

1253 

Gastrocnemius. 

II 

Soleus. 

Sacral 

Tibialis  posticus. 

Detrusor  urinae. 

and  other 

All  the  small  mus- 

muscles as 

cles  of  foot. 

in  3d  sacral. 

Ejacula- 
tion lost. 
Erection 
diminished. 
Tendo- 
Achillis 


None 


Defecation  dis- 
turbed. 
Retention  of 
urine  later 
followed  by 
dribbling. 
Ejaculation  lost. 
Erection  possible 
but  paretic. 


Outward  rotation   Ejacula-  None, 
of  tliigh.  tion. 

Retraction  of  thigh.  Erection. 
Flexion  of  knee.     Plantar 
Plantar  flexion  of  weakened, 
foot. 

Standing  on  the  toes. 
Rai.sing  inner  margin 
of  foot- 
Defecation  and 
Retention  of  urine 
as  in  3d  sacral. 


Skin  over  sac- 
rum and  anus. 


Slightly  larger 
area  than  above 
extending  over 
inner  portion 
of  gluteal 
region. 


As  above,  and 
perineum,  gen- 
itals and  upper 
part  of  inner 
surface  of 
thighs. 

(Testicle  sensi- 
tive to 
pressure). 

As  above,  and 
the  posterior 
surface  and 
outer  surface 
of  thighs. 


220 


TABLE  OF  SYMPTOMS  IN  TRANSVERSE  LESIONS  AT  DIFFERENT  LEVELS  OF 

THE  CORD  (Continued) 


Modified  from  Wichman 


Segment 
Involved 


Motor  Conditions 


Reflex 
Conditions 


Sensory 
Conditions 


>%». 


1254 

I 
Sacral 


1255 
V 
Lum- 
bar 


Paralysis 

Muscles  of 

anus. 

Muscles  of 

bladder. 

Muscles  of 

genitals. 

Pyriformis. 

Abductor 

halluds. 

Flexor 

hallucis 
■i  brevis. 

T-IV  dorsal 

interossei. 

I -1 1 1  plantar 

interossei. 

III-IV  lum- 

bricales. 

Abductor 

minimi 

dijfiti. 

Onponens 
.  minimi  digiti. 


Paresis 


1 


Muscles  of  anus 

and  rectum. 

Muscles  of 

bladder. 

Muscles  of 

genitals. 

Pyriformis. 

Biceps 

femoris. 

Flexors  of 

toes. 

Peroneus 

longus. 

Peroneus 

brevis. 


Gluteus  maj^mus. 
Obturator  intemus. 
Gemellus  superior. 
Gluteus  medius. 
Gluteus  minimus. 
Biceps  femoris. 
Semimembranosus. 
Semitendinosus. 
Popliteus. 
Gastrocnemius. 
Soleus. 

Tibialis  f)osticus. 
Peroneus  longus. 
Peroneus  brevis. 
Flexors  of  toes. 
Extensors  of 
toes. 

Gemellus  sui)erior. 
Gemellus  inferior. 
Gluteus  medius. 
Gluteus  minimus. 
Semimembranosus. 
Semitendinosus. 
Gluteus  miximus. 
Tensor  fasciae 
femoris. 
Gastrocnemius. 
iSoleus. 

Extensors  of  toes- 
Tibialis  anticus. 


Actions  lost  or 
impaired 


Absent 


.  Anesthesia 

In-  with  a  zone  of 

creased  hyperesthesia 

in  surrounding 

partial  it  or  limiting 

lesions  it  above 


tu 


Retention  of  feces. 
Retention  of  urine 
or  dribbling. 
Erection  and  ejacu- 
lation impiossible. 
Outward   rotation 
of   thigh  im- 
paired. 

Internal  rotation 
impaired. 
Flexion  of  knee 
difficult. 

Plantar   flexion   of 
foot. 

Raising  inner  mar- 
gin of   foot. 
Raising  outer  mar- 
gin and  dorsal 
flexion  of  foot. 
Flexion  and  extension 
of  toes,  adduction  of 
great  toe,  abduction 
of  little  toe,  etc. 


Defecation. 
Micturition  delayed, 
dribbling. 

Erection  and  ejacu- 
lation impossible. 
Outward   rotation 
of  thigh  very 
difficult. 

Inward   rotation 
impaired. 
Flexion  of  knee 
difficult. 

Retraction  of  thigh 
very  difficult. 
Flexion  of  foot 
barely  possible. 
Flexion  of  toes 
impossible. 
Extension  of  toes 
weak,  except  great 
toe,  which  may  be 
dorsally  flexed. 
Raising  inner  margin 
of  foot  difficult. 
Raising  outer  mar- 
gin of  foot  im- 
possible. 


Plantar      None 
weakened. 
Achilles- 
tendon 
reflex. 
Ejaculation. 
Erection. 
Micturition. 
Defecation. 
Gluteal. 


As  above,  and 
a  strip  on 
posterior  and 
outer  surface 
of  lower  legs 
and  of  dorsum 
of  foot  and 
especially  of 
toes. 


Ejacu-      Plan-  As  above,  and 

lation.        tar.  back  of  thighs 

Erection.  Tendo-  and  legs  and 

Achil-  inner  and  outer 

Us-  margin  and 

Micturition.  sole  of  feet. 
Defecation. 
Gluteal. 


221 


TABLE  OF  SYMPTOMS  IN  TRANSVERSE  LESIONS  AT  DIFFERENT  LEVELS  OF 

THE  CORD   (Continued) 


Modified  from  Wichman 

Segment 

Reflex 

Sensory 

Involved 

Motor  Conditions 

Conditions 

Conditions 

-( 

In- 
creased 
in 

>  Anesthesia 
with  a  zone  of 
hyperesthesia 
surrounding 

Actions  lost  or 

partial 

it  or  limiting 

Paralysis 

Paresis 

impaired 

Absent 

lesions 

it  above 

Muscles  of  rec- 

Defecation, with 

Patellar 

Plan- 

As above,  and 

tum  and  anus. 

fecal  incontinence. 

may  be 

tar. 

inner  side  of 

Muscles  of 

Micturition,  with 

wanting. 

lower  l^s  and 

bladder. 

dribbling. 

dorsum  of  feet 

Muscles  of 

Erection  and  ejacu- 

and strip  on 

genitals. 

lation  impossible. 

outer  posterior 

Obturator 

Outward  rotation  o; 

E 

surface  of 

internus. 

Obturator 

thigh  weak. 

thighs. 

Pyriformis. 

internus. 

Inward  rotation 

Gemelli. 

impossible. 

Gluteus 

Retraction  of  thigh 

medius. 

impossible. 

1256 

Gluteus 

Flexion  of  knee 

IV 

minimus. 

lost. 

Lum- 

Gluteus 

Plantar  flexion  of 

bar 

maximus. 
Biceps 
femoris. 
Semi- 
membranosus. 
Semi- 
tendinosus. 
Popliteus. 
Gastrocne- 
mius. 
Soleus. 
Flexors  of 
toes. 

Extensors  of 
toes. 

Peroneus 
brevis. 
Peroneus 
lonsTis- 
Tihialis 
anticus. 

Rectus   femoris. 
Vastus  extemus. 
Va.stus  intemus. 
Adductor  magnus. 
Adductor  brevis. 
Adductor  minimus. 
Gracilis- 

foot  lost. 

Flexion  and  exten- 
sion of  toes  lost. 
Raising  outer  mar- 
gin of  foot. 
Raising  inner  mar- 
gin. 

Extension  of  thigh 
weak. 
Adduction   difficult. 

Muscles  of 

Vastus  internus. 

All  movements  of 

Patellar 

Ankle- 

As  above,  and 

anus,  bladder 

Rectus  femoris. 

legs  are  lost,  except  and 

clonus 

whole  of  legs 

and  genitals. 

Crureus. 

that  extension  of 

cremas- 

may 

except  a  tri- 

Outward ro- 

Adductors of  thigh 

.  legs  is  barely  pos- 

teric. 

exist. 

angular  area  on 

tators  of 

Flexors  of  thigh 

sible  and  that  the 

front  of  thigh 

thigh. 

at  the  hips. 

thigh  can  be  flexed 

with  base  at 

It! ward  rota- 

on body  by  the 

Poupart's 

1257 

tors  of  thigh. 

psoas  and  iliacus. 

ligament. 

Retractor  of 

Defecation  and  mic- 

III 

(flexor)    thigh. 

turition  are  de- 

Lum- 

Flexors of  knee. 

stroyed. 

bar 

Plantar   flexors 

Urine  and  feces 

of  foot. 

dribble  and  cannot 

Flexors  of  toes. 

be  retained- 

Extensors  of 

foot. 

Vastus  extemus. 

222 


TABLE  OF  SYMPTOMS  IN  TRANSVERSE  LESIONS  AT  DIFFERENT  LEVELS  OF 

THE  CORD  (Continued) 

Modified  from  Wichman 


Involved 

Segment 


Paralysis 


Motor  Conditions 


sisaaBj 


Actions  lost  or 
impaired 


Reflex 
Conditions 

In- 
creased 
in 

partial 
Absent     lesions 


1258 

Paralysis  of 

•SBOSJ 

II 

all  muscles 

Lum- 
bar 

of  lower 
extremity, 
except  psoas. 

1259 

Total  paralysis 

I 

of  whole  lower 

Lum- 

extremity. 

bar 

psoas  included. 

Paralysis  of 
lower  extrem- 

1260 

ity,  and  gluteal 

XII 

region. 

to  III 

Paralysis  of 

Dor- 

abdominal 

sal 

and  dorsal 
regions,  gradu- 
ally added  as 
the  site  of  the 
lesion  ascends. 

1261 

As  in  3d 

II 

dorsal. 

Dor- 

sal 

1262 

All  muscles 

Flexion  of  fingers. 

I 

of  trunk  and 

Muscles  of  the  little 

Dor- 

lower ex- 

finger. 

sal 

tremities. 

Ill  and  IV  inter- 

SBOS(j  Complete  paralysis 
of  legs,  rectum 
and  bladder. 


As  above. 


As  above. 


ossei. 

Lumbricales. 
Pronator  quadratus. 
Lower  part  of  pec- 
toralis  major. 
Lower  part  of  pec- 
toralis  minor. 


As  above. 


As  above  and 
weakness  in 
flexion  of  fingers. 
Pronation  dis- 
turbed. 


PateUar, 
Achilles 
and 

cremas- 
teric. 


Achil- 
les 
may 
be  in- 
creased. 
Plantar. 


Sensory 
Conditions 

^  Anesthesia 
with  a  zone  of 
hyperesthesia 
surrounding 
it  or  limiting 
it  above 

Whole  of  legs 

and  pelvis. 

(Testicles  not 
sensitive  to 
pressure.) 


As  above,  and 
paralysis  of  mus- 
cles of  respiration 
causes  diaphragm- 
atic breathing  and 
dyspnoea. 


Cremas-   Patel- 
teric  and  lar  ab- 
Achilles.  sent  or 
"in- 
creased. 

Epigas-     Patel- 
tric  and    lar, 
umbilical  cre- 
reflex.       mas- 
teric, 
Acliil- 
les  and 
plan- 
tar. 


All  below 
lost  in 
complete 
division 
of  cord. 


All 

subja- 
cent 
re- 
flexes. 


Oculo-      All 
pupillary  subja- 
symp-       cent 
toms.        re- 

■■  *  flexes- 
All  below 
lost  in 
complete 
division 
of  cord. 


As  above,  and 
groins  and  front 
of  scrotum  and 
penis. 


As  above,  and 
a  band  running 
around  body 
about  two  seg- 
ments below 
the  one  in- 
volved and 
limited  above 
by  a  narrow 
zone  of  hyper- 
esthesia. 


As  above,  and 
a  strip  on  the 
inner  side  of  the 
upper  arms. 


As  above,  and 
a  strip  on  the 
inner  side  of  the 
forearms. 


223 


TABLE  OF  SYMPTOMS  IN  TRANSVERSE    LESIONS    AT    DIFFERENT  LEVELS 

OF  THE  CORD  (Continued) 

Modified  from  Wichman 


Segment 

Reflex 

Sensory 

Involved 

Motor  Conditions 

Conditions 

Conditions 

Anesthesia 
with  a  zone  of 

In- 

creased 

hyperesthesia 

■^                           in 

surrounding 
it  or  limiting 

Actions  lost  or 

^                          in 

>artial 

Paralysis 

Paresis 

impaired 

Absent       esions 

it  above 

Paralysis  of 

Flexors  of  the  lit- 

.\s above. 

Oculo-      All 

As  above,  and 

muscles  of 

tle  finger. 

pupillary  below. 

the  fingers, 

trunk  and 

Opponens  minimi 

symp- 

except volar 

lower  extrem- 

digiti. 

toms. 

surface  of  the 

1263 

ities. 

Flexor  subl.  digi- 

thumb  and  the 

Vlll 

Abductor  of 

torum. 

ulnar  surface 

Cer- 

little finger. 

Flexor  pro  fun.  digi 

- 

All  below 

of  the  little 

vical 

Adductor  of 

torum. 

lost  in 

finger. 

thumb. 

Flexor  carpi  ulna- 

complete 

Flexor  of  the 

ris. 

division 

The  cervical 

little  finger. 

Extensors  of  the 

Hand  weak. 

of  cord. 

sensory  nerve 

Opponens 

thumb  and  fingers. 

roots  supply  the 

minimi  digti 

Triceps   (slight). 

Extension  of  arm. 

same  area  of  the 

III  and  IV 

Latissimus  dorsi 

Int.  rotation  and 

skin  in  common, 

interossei. 

(lower  part). 

retraction  of  arm. 

especiallv  in  the 

Lumbricales. 

Pectoralis  major. 
Pectoralis  minor. 
Scalenus    medialis. 
Scalenus  posticus. 

Adduction  of  arm 

hands  and  fin- 
gers. Hence  the 
anesthesia  is 
slight  and  un- 
certain. 

Lower  ex- 

Extensors, 

As  above  and 

Arm         All 

As  above,  and 

tremities  and 

Flexors 

Hand  very  weak. 

reflexes,   below. 

most  of  the 

trunk. 

and 

Retraction  and  in- 

Forearm 

hands  and  a 

Flexor  pro- 

Abductors 

ward  rotation  of 

reflexes. 

.small  strip  on 

fundus  digi- 

of  thumb. 

arm. 

Palmar 

the  anterior. 

1264 

torum   (ulnar 

Exte:isor  indicis. 

(Winged  scapulae" 

)  reflex. 

another  on  the 

VII 

side). 

Extensors  of  the 

posterior,  sur- 

Cer- 

Flexor carpi 

fingers  (movements 

face  of  the 

vical 

ulnaris. 

barely  possible). 

All  below 

foreanr). 

Small  hand 

Supinator  longus. 

lost  in 

muscles. 

Biceps  (very  slightly 

complete 

Pronator 

paretic. ) 

cord 

quadratus. 

Triceps 

Pectoralis  major. 
Serratus  magnus 
(slight). 

Latissimus  dorsi. 
Teres  major. 

division. 

224 


TABLE  OF  SYMPTOMS  IN  TRANSVERSE  LESIONS  AT  DIFFERENT  LEVELS  OF 

THE  CORD  (Concluded) 

Modified  from  VVichman 


Se 

NSORY 

Reflex 

Conditions 

Conditions 

Motor  Conditions 

Conditions 

Sensory 

^  Anesthesia 

t -*■ 

In- 

with a  zone  of 

creased 

hyperesthesia 
surrounding 

f 

"^                 in 

Actions  lost  or 

partial 

it  or  limiting 

Paralysis 

Paresis 

impiiired 

Absent      lesions 

it  above. 

Muscles  of 

Coraco-brachialis. 

As  above  and 

Arm          All 

As  above,  and 

lower  extrem- 

Biceps. 

movements  of  fin- 

reflexes,   below. 

whole  of  hands 

ity  and  trunk. 

Bracliialis   anticus. 

gers  and  thumb 

Extensor 

and  fingers  and 

^luscles  of 

Supinator  brevis. 

impossible. 

forearm 

radial  side  of 

fingers  (in- 

Deltoid. 

Extension  of  fore- 

reflexes. 

forearm. 

1265 

cluding  thumb) 

Scaleni. 

arm. 

VI 

and  hand. 

Splenii. 

Flexion  of  forearm 

Cer- 

Triceps. 

Deep  head  and 

weak. 

All  below 

xncal 

Pectoralis 

neck   muscles. 

Supination  very 

lost  in 

major. 

weak. 

complete 

Latissimus 

Adduction  of  arm 

cord 

dorsi. 

and  inward  rota- 

division. 

Teres  major. 

tion. 

Infraspinatus. 

Adduction,  retrac- 

Serratus 

tion  and  external  ro 

'- 

magnus. 

tation. 

(Winged  scapulae.) 
Raising  of  arm. 
Rotation   of   head'. 
Fatal  in  a  few  days 
or  weeks. 

Muscles  of 

Levator  anguli 

As  above  and 

Scapular     .All 

As  above,  and 

lower  extrem- 

scapulae. 

shoulders  raised 

and              below. 

whole  of  arms, 

ities  and 

Scaleni. 

with   difficulty 

tendon 

except  tip  of 

trunk. 

Diaphragm    ( be- 

Rotation and  flex- 

reflexes of 

shoulder. 

.■Ml  the  mus- 

cause of  filaments 

ion  of  head. 

paralysed 

cles  of  the 

from  V  cervical  seg- 

Dyspnoea. 

muscles 

1266 

arm.  forearm, 

ment  to   phrenic 

Fatal  in  a  few 

in  arms. 

V 

hand  and  fin- 

nerve), or  spread  of 

hours  or  days. 

Cer- 

gers; even  the 

injury   from  5th 

vical 

deltoid, 

to  4th  cervical 

-All  below 

coraco- 

segment. 

lost  in 

brachialis  and 

Trapezius  and 

complete 

brachialis 

sterno-cleido-mas- 

cord 

anticus. 

toid  are  int.ict. 

divi-sion. 

Deep  cervi- 

cal muscles. 

Intercostals. 

1267  Total  cross-lesions  from  the  fourth  cervical  segment  upward  are  rapidly  fatal,  because 
iV-I  of  complete  paralysis  of  the  diaphragm  and  intercostals. 
Cer- 
vical Total  cross-lesions  of  the  brain-stem  are  rapidly  fatal  for  the  same  reason. 


22: 


B.— TABLE  OF  SYMPTOMS  ACCORDING  TO  AREA  INVOLVED  IN  TRANSVERSE 
SECTION  OF  THE  SPINAL  CORD 


1268     Lesions  of  anterior  horns,     i 


Acute  anterior  poliomyelitis    (495,  789,  1148,  1233,  1324.) 
Chronic  atropluc  paralysis  (547-8,  695,  1150,  1324.) 

1269  Lesions  of  posterior  horns;  sensory  disturbances  (1322.) 

1270  Lesions  of  pyramidal  tract;  Spastic  Paraplegia  (525-47,  800,  1212,  1384-6-9,  1406.) 

1271  Lesions  of  posterior  columns;  Tabes  (661,  785-6,  1322,  1360,  1363-4,  1406.) 

1272  Lesions  of  direct  cerebellar  tracts;  Hemiataxia  (653.) 

1273  Lesions  of  postero-lateral  columns;  Ataxic  Paraplegia  (526,  660,  799,  1360,  1406.) 

1274  Lesions  of  spino-thalamic  tract;   Dissociation  of    sensation  (812,  1369.) 

1275  Lesions  of  anterior  gray  commissure;  Syringomyelia  (552,  693,  798,  840-2,  1370-2.) 

1276  Lesions  of  entire  lateral  half ;  Brown-Sequard  paralysis  (442,  509,  844,  975-82.) 

1277  Lesions  of  posterior  spinal  ganglion;  Herpes  Zoster  (940,  978,  1166,  1235.) 

1278  Lesions  of  posterior  nerve  roots;  Tabes  a:id  Herj>es  Zoster. 

1279  Lesions  of  anterior  nerve  roots;  Atrophic  paralysis. 


226 


CHART  XXI 

Cerebral  Localization 

Comprising  Numbers  1290  to  1309 


227 


CHART  XXIa 

Cerebral  Localization  in  the  Medulla  and  Pons* 

Ganglia  at  Base 

Comprising  Numbers  1290  and  1292 


229 


Seat  of  Lesion 

1290 

r.esion    involving    latoral    half   of    the    Medulla 
Oblonsata :     Avellis'  syndrome. 


Babinski 
(427). 


and     Nageotte's     Bulbar     Syndrome. 


liarc  because  of  the  small  transverse  area  of  the 
ni-<lulla    (Fig.  22). 


TJitl 

Thrombosis    of    Posterior    Inferior    Cerebellar 
.\rtcry.     (Figs.  21-3). 


1292 

Lesion     in     lat- 
eral    half    of. 
the  Pons 
Varolii. 
(Fig.  20.) 


Lesion  in 
Lower 
(Caud.nd) 
Third. 


Confined   to   the 
bridge  por- 
tion. 


Confined   to   the 
tegmentum. 


Ijesion  in 
Middle    and 
Upper 
(Cephalad) 
Thirds. 


Confined   to   the 
bridge  por- 
tion. 


Confined   to   the 
tegmentum. 


Paralysis  of 
Motion 

Crossed  paralysis :  hemiple- 
gia alternans  hypoglos- 
sica.  Homolateral  half  of 
tongue,  diaphragm  and 
vocal  cord,  contralateral 
arm  and  leg.  In  some 
cases  arm  and  leg  may  be 
paralysed  on  both  sides, 
but  not  equally  so.  Ex- 
tremely rarely  leg  on  one 
side  and  arm  on  the  other 
are  paralysed. 

None. 


Crossed  paralysis :  hemiple- 
gia alternans  facialis. 
Muscles  of  expression  of 
homolateral  half  of  face 
and  the  external  rectus  at 
times,  and  contralateral 
arm,  leg  and  half  of  tongue 
(Millard-Gubler's  syn- 

drome— 429). 

Muscles  of  expression  of 
homolateral  half  of  face 
and  of  external  rectus 
(Foville's  paralysis — 454). 
Contralateral  internal  rec- 
tus and  arm  and  leg  may 
be  slightly  involved. 


Complete  contralateral  hemi- 
plegia. 


Conjugate  deviation  of  eye- 
balls toward  the  side  of 
the  lesion.  May  be  com- 
plete hemiplegia  of  slight 
degree  from  pressure. 


TABLE   OF   SYMPTOMS    IN   TBANSVERi 
LOCALIZATION   IN   MEDU 


Action  Lost  oe 
Impaibed 

-\rtieulation,  phonation,  de- 
glutition, respiration,  car- 
diac action.  coughing, 
vomiting,  use  of  tongue 
and  of  arms  and  leg  on 
one  or  both  sides. 


Paralysis  op 
Sensation 

Taste  in  posterior  part  of 
homolateral  half  of 
tongue.  All  forms  of  sen- 
sation in  pharynx  and 
throughout  the  respira- 
tory tract.  Analgesia  and 
thermic  anesthesia  of 
homolateral  half  of  face 
and  contralateral  half  of 
body,  .\nesthesia  of  one 
side,  or  of  both  sides  of 
the  body. 


Analgesia,       thermic      anes-      Deglutition,    articulation, 
thesia     and      tingling     in 
homolateral    side    of    face, 
tongue  and  nostril,  and  in 
contralateral  arm  and  leg. 


None,  unless  indirectly  from 
pressure  and  then  contra- 
lateral  hemianesthesia. 


Contralateral  hemianalgesia 
and  thermic  anesthesia 
and  at  times  hemianes- 
thesia. Anesthesia,  and 
especially  analgesia,  of 
homolateral  half  of  face 
(Hemianesthesia  altern- 
ans). Very  rarely,  deaf- 
ness. Rarely  dissociation 
of  sensation. 

Usually  of  all  forms  of  sen- 
sation in  homolateral  half 
of  face.  Occasionally  also 
hemianesthesia  of  contra- 
lateral half  of  body. 


Paralysis  of  all  forms  of 
sensation  on  homolateral 
half  of  face.  Contralateral 
hemianalgesia.  May  be 
contralateral  hemianes- 
thesia. 


.\rtirulation.  winking,  mas- 
tication. Movements  of 
homolateral  half  of  face, 
and  of  contralateral  arm 
and   leg. 


.\rticuIation,  mastication, 

winking.       Movements     of 
homolateral  half  of  face. 


Chewing  and  usually  articu- 
lation. Movements  of  con- 
tralateral half  of  body. 


Chewing  and  usually  articu- 
lation. Conjugate  move- 
ment of  eyeballs  toward 
the  same  side  as  the 
lesion. 


LESIONS   OF   BRAIN-STEM 
AND   PONS 

Reflexes 
Altered 


cndon  reflexes  lncreaS(Ml 
with  Babinski  and  ankle- 
clonus  on  opposite  side. 
Cutaneous  reflexes  may  or 
may  not  be  increased. 


llsun 


Muscle 

Vicr.Tir.o 

Ataxia 

Sense 

ly    present. 

T'sually  present 

Usually   lost,   espe 

and   of   both 

cially  if  motor 

motor    and    cere- 

ataxia be 

bellar   type. 

present. 

Homolateral. 

Secretort  and 
Other  Disturbances 

Miosis      and      pseudo-ptosis 
(ophthalmoplegia  sym- 

pathiea)      and     salivation 
are     common.  Cheyne- 

Stokes's    respiration  (42J)). 


formal     except     in 
cranial  nerve.s. 


certain 


'endon  reflexes  increase<l 
with  Rabinski  and  ankle- 
clonus  on  opposite  side. 
Cutaneous  reflexes  may  or 
may  not  be  increased. 


Usually  present   at 
onset. 


Often  present. 


Extreme  in  homo- 
lateral arm  and 
leg. 


Xo   motor,   but 
there  may  be 
cerebellar, 
ataxia. 


Lost  in  homo- 
lateral arm 
and  leg. 


Normal. 


Increased  secretion  of  sweat 
in  contralateral  side.  Ten- 
dency to  fall  towards  the 
side  of  the  lesion.  Nys- 
tagmus frequent. 

Conjunctivitis  is  frequent  in 
eye  of  same  side.  May  be 
a  tendency  to  fall  or  to 
turn  to  one  side.  Saliva- 
tion. 


orinal    or   slightly   exasger- 
ated  as  above. 


Usually    present. 


Usually  present  on 
the  same  side  as 
the  lesion. 


T-iOSt    on    the    same 
side    as    the 
lesion. 


Conjunctivitis  is  frequent  iu 
the  eye  of  the  same  side 
Salivation. 


I'lidoii  reflexes  increased 
with  Babinski  and  ankle- 
clonus  on  the  opposite 
side.  Cutaneous  reflexes 
may  or  may  not  be  in- 
creased. 


Often    present. 


No   iiMtor.   may   be      Normal. 
cerebellar, 
ataxia. 


Ulceration  of  cornea  ma.v 
occur.  May  be  a  tendency 
to  fall  or  turn  to  one  side 


ormal    or    may   be    slightly       Present. 
e\'aggerate<l. 


May  be  motor  and 
cerebellar 
ataxia. 


Lost    on    the   same 
side  as  the 
lesion. 


Ulceration  of  the  cornea 
may  rarely  occur.  A  slow 
rhythmic  tremor  of  the 
arm  and  leg  of  opposite 
side  may  be  present. 


CHART  XXIb 

Cerebral  Localization:  Ganglia  at  Base 

TABLE  OF  SYMPTOMS  IN  TRANSVEESE  LESIONS  OF  BRAIN  STEM  AND   CEREBELLUM 

.\CTioNs  Secretory 

Paralysis  of       Paralysis  of  Lost  ob  Altered  Ver-  .Muscle      and  Other 

Seat  of  Lesion  Motion  Sensation  Impaired         Reflexes  tigo  Ataxia     Sense     Disturbances 


Some,  or  all,  of 

None. 

Movement 

Tendon 

Usually 

None. 

Normal. 

Tremor 

the  ocular  mus- 

of eye- 

reflexes 

absent. 

resembling 

cles    (except 

ball.     Use 

increased. 

that  of 

external  rectus) 

of  contra- 

with 

paralysis 

on    the   same 

lateral 

Babinski 

agitans  of 

•Lesion 

side,    combined 

half  of  the 

and   ankle- 

contralateral 

confined 

with  a  contra- 

body. 

clonus,  on 

arm   and  leg 

to  the 

lateral   hemiple- 

opposite 

(Benedikt's 

pes  or 

gia,   usuall.v 

.side. 

syndrome) . 

foot. 

complete. 
Hemiplegia 

Cutaneous 
reflexes 

('431) 

alternans 

Contralateral 

may  or 

oculomotoria. 

hemianesthesia, 

may  not 

(Weber's    syn- 

or   hemi 

analge- 

be   in- 

A slow. 

drome,  430). 

sia  and 

thermic 

creased. 

rhythmic 

hemianesthesia, 

tremor  of 

Lesion 

One  or  more 

or  both. 

Deaf- 

Movement 

Tendon 

Present. 

Cere- 

Im- 

arm and  leg 

confined 

ocular  muscles. 

ness  may  be 

of  eyeball. 

reflexes 

bellar 

paired. 

of  opposite 

to  the 

except  the 

present. 

if 

normal. 

type. 

side  may  be 

tegmen- 

abducens. 

lesion  be 

present. 

.tum. 

bilateral 

m  ^^>^^ 

'Lesion 

BUateral.    more 

May  be  blind- 

Movement 

Pupil 

Usually 

May   be 

Normal. 

Nystagmus     (at 

confined 

or  less  exten- 

ness  without 

of  eyeball. 

reflex  lost 

absent. 

absent. 

times   vertical). 

to 

sive,  of  all  ocu- 

choked disc  or 

to  both 

squint,  pupils 

anterior 

lar  muscles. 

other  lesion. 

light  and 

often    unequal. 

pair 

except    the 

accommo- 

(nates). 

abducens. 

dation. 

May   be  slow, 

Lesion 

None  or  may 

May  be 

deaf- 

None, 

Normal. 

Usually 

Present. 

Normal. 

rhythmic 

confined 

be  slight 

ness,  if 

lesion 

except 

present. 

Of   cere- 

tremor  of   arm 

to 

paralysis    as 

be   bilateral. 

chewing 

bellar 

and  leg  of 

posterior 

above,  or  of 

at  times. 

type. 

opposite   side. 

pair 

trochlearis. 

especially  on 

.(testes). 

voluntary 
motion. 

None. 

None. 

Walking 

Normal 

Usually 

Cere- 

Normal. 

Nystagmus 

and 

or 

present. 

bellar 

(SO),    tendency 

standing 

slightly 
exagger- 
ated. 
R.irely 
abolished. 

ataxia 
wiUi 
hypo- 
tonia 
almost 
always 
present. 

to   fall    to   one 
side,  occipital 
headache  is 
frequent, 
cerebellar 
fits  may 
occur. 

None. 

None. 

Walking, 

Normal 

Usually 

Usually 

Normal. 

Tendency    to 

standing 

or 

present. 

present 

fall  or  to   turn 

and 

slightly 

with 

eyes,  head  or 

sitting. 

exagger- 
ated. 

hypo- 
tonia 
of  the 
cere- 
bellar 
type. 

body   to  one 
side.     Rotatory 
movements, 
more  or  less 
pronounced, 
choreic-spasms 
in  homolateral 

Lesion 

of  iiif(>rior  cerebellar  pedu 

Qcles  cause  lateropulsion ;    those  of  the  su- 

half  of  body. 

perior   ■erelu'llar    peduncles   cause   choreiform    movements    and   cerebellar 

and   vertical 

ataxia. 

divergence    o£ 

the  eyeballs 

sometimes 

occur. 

Fractures,  tumors,  etc.,  at  base  of  skull  may  cause  many  of  the  above  symptoms  according  to  their  position,  but 
their  early  and  characteristic  symptom  is  paralysis  of  one  or  more  of  the  cranial  nerves.  Symptoms  of  pa- 
ralysis predominate  over  those  of  irritation. 

Small  lesions,  not  so  extensive  as  to  involve  the  entire  lateral  half  of  the  brain  stem,  may  occur  at  any  point. 
The  symptoms  of  these  lesions  depend  upon  the  function  (physiology)  of  the  part  affected  and  will  naturally 
vary  greatly.  The  location  of  such  a  lesion  in  a  transverse  section  will  depend  upon  what  longitudinal  fiber 
tracts  are  involved,  and  in  longitudinal  section  upon  what  cranial  nuclei  and  nerve  tracts  are  involved,  aa 
shown  by  the  symptoms  present  in  any  case.  A  study  of  the  figures  at  the  end  of  this  book  is  essential  for  the 
localization  of  such  lesions  and  will  serve  this  purpose  better  than  a  long  verbal  description. 

231 


CHART  XXIc 
Cerebral  Localization:  Ganglia  at  Base 

LOCALIZING  SYMPTOMS  IN  LESIONS  OF  GANGLIA  AT  BASE  OF  BRAIN 


Seat  of  Lesion 

1298 

Optic  Thalamus. 

(Fig.  17)  (837a) 


Nucleus 

Lentic- 

ularis 

and 

Nucleus 

Cauda- 

tus. 


1299 
Corpus 
Stri- 
atum. 
(Fig.  17) 


Inter- 
nal 
Cap- 
sule. 


1300 

Corpus  Callosum. 

1301 

Island  of  Riel 
Qau  strum  and 
External  capsule. 
(Fig.  17) 

1302 

Pituitary  Gland. 


1303 

Pineal  Gland. 


Diagnostic  Symptoms 
Is  the  highest  and  most  important  center  for  complicated  automatic  actions.  It  is 
the  seat  of  the  emotion  of  anger  and  probabl}',  in  large  part  of  pleasure  and  well 
being.  Disease  of  tliis  organ  may  give  rise  to  few  characteristic  symptoms. 
There  may  be  hemiaiiopia  (pulvinar  and  external  geniculate  involvement)  vrith 
hemiopic  pupillary  reaction  and  contralateral  sensory  disturbances  with  conse- 
quent incoordination.  In  lesions  of  the  optic  thalamus  occasionally  a  slight  irri- 
tation of  the  skin  is  not  felt  at  all,  while  a  stronger  one  is  felt  inordinately. 
Absence  of  emotional  expression  in  face,  even  when  not  paralysed.  Vaso-motor 
disturbances  may  occur  in  opposite  side  of  body.  Isolated  analgesia  and  thermic 
anesthesia  do  not  occur  in  lesions  above  the  optic  thamus. 

In  rare  cases  a  lesion  of  the  nucleus  lenticularis  may  be  of  such  a  form  as  to  injure 
the  anterior  and  posterior  part  of  the  posterior  limb  of  the  internal  capsule,  while 
its  middle  part  escapes.  In  such  cases  there  results  a  hemiplegia  which  involves 
the  leg  and  face  more  than  the  arm.  Dysarthria  is  a  not  uncommon  symptom 
and  in  some  cases  the  symptoms  of  sensory  irritation  and  incoordination  described 
under  lesions  of  the  optic  thalamus  have  been  present.  When  the  ganglia  on 
both  sides  are  affected,  voluntary  voiding  of  urine  may  be  impossible,  while  au- 
tomatic involuntary  voiding  may  occur  at  regular  intervals.  The  most 
characteristic  s\Tnptoms  due  to  lesions  in  the  corpus  striatum  are  rigidity  ( Park- 
inson's disease^— 677),  choreiform  movements  (Huntington's  chorea — 624)  and 
athetosis  ( Post-hemiplegic — 632  and  Bilateral — 631).  These  symptoms  aisp 
form  part  of  the  syndromes  known  as :  pseudo-sclerosis — 667,  progressive  lenti- 
cular degeneration  and  dystonia  lenticularis   (668). 

'  Lesions  in  the  anterior  limb  of  the  internal  capsule  cause  either  no  symptoms  or  a 
paralysis  of  contralateral  half  of  face.  There  may  be  ataxia  and  athetoid  move- 
ments. 

Lesions  in  the  anterior  two-tliirds  of  the  posterior  limb  of  the  internal  capsule 
cause  a  total  contralateral  hemiplegia  of  the  body.  This  hemiplegia  consists 
purely  of  a  muscular  paralysis  and  never  produces  a  paralysis  of  the  cortical 
functions  such  as  aphasia,  alexia,  etc;  but  may  produce  dysarthria. 

Lesions  in  the  posterior  third  of  the  posterior  limb  of  the  internal  capsule  cause 
hemianesthesia  and  loss  of  muscle  sense  on  the  opposite  side  of  the  body. 

Lesions  at  the  extreme  posterior  end  of  the  posterior  limb  of  the  internal  capsule, 
in  addition  to  hemianesthesia,  cause  contralateral  hemianopia,  deafness,  only  if 
the  lesion  be  bilateral,  and  often  the  symptoms  of  motor  irritation,  described 
under  lesions  of  optic  thalamus. 

No  diagnostic  symptoms.  Symptoms  of  ingravescent  character,  gradual  develop- 
ment of  hemiplegia,  with  slight  hemiplegia  of  the  other  side  also,  drowsiness, 
dysarthria  and  anarthria.     Death  in  coma  (Bristow's  syndrone). 

Lesions  in  this  area  produce  disturbances  of  speech,  grouped  under  the  general 
term  paraphasia,  and  may  produce  anarthria,  the  result  of  complete  aphasia. 

Hypertrophy,  tumor,  hemorrhage  and  some  other  lesions  of  the  gland  associated 
with  excess  of  secretion  may  cause  acromegaly  or  gigantism,  in  addition  to  a 
progressive  bi-temporal  hemianopia,  terminating  in  blindness.  A  defect  or 
atrophy  of  the  gland  associated  with  a  diminution  of  secretion  in  early  life  may 
cause  dwarfism  and  may  produce  pituitary  eunuchismus  or  adiposogenital  de- 
generation with  excess  of  fat  and  a  defect  in  the  formation  of  the  genitals.  In 
any  case  of  pituitary  disease  there  may  be  polyuria,  polydipsia  and  occasionally 
glycosuria  and  very  rarely  an  escape  of  cerebro-spinal  fluid  from  the  nose 
(hydrorrhoea  nasalis).  In  some  cases  of  pituitary  disease  there  are  no  symp- 
toms. 

Abnormal  growth  of  hair  and  deposition  of  fat.  Abnormalities  of  genitals  (at 
times  with  attacks  of  sexual  excitement,  eunuchismus).  Excessive  growth  in 
height  of  body  (dyspinelismus).  In  consequence  of  involvement  of  adjacent 
tissue,  bilateral  ocular  paralysis,  nystagmus,  pupil  abnormalities,  ataxia,  and  per- 
haps disturbances  of  hearing  may  be  present. 

233 


CHART  XXId 
Cerebral  Localization:  Lobes  of  Brain 


LOCALIZING  SYMPTOMS  IN  LESIONS  OF  CEREBRAL  HEMISPHERES 


Seat  of  Lesion 

1304 

FRONTAL  LOBE 
Contains  the  centers 
for  all  the  skilled 
acts,  especially  the 
left  lobe.  Large 
lesions  in  the  frontal 
lobes  may  cause  a 
change  in  character 
and  disposition  of 
the  patient.     Many 
lesions,  especially 
tumors,  cause 
Jacksonian  epilepsy, 
especially  when  sit- 
uated in  posterior 
part  of   lobe ;   while 
lesions  in  anterior 
part  of  lobe  may 
cause  epileptiform 
convulsions.     Ataxia 
sometimes  occurs  in 
tumors  in  the  fron- 
tal lobe.     (Fig.  15) 


rThe 
ascending 
frontal 
convo- 
lution. 

Lesions 

in  this 

region 

may 

cause 

awkward- 


ness 

( cortical 

ataxia  or 

apraxia) 

rather  than 

paralysis. 


Diagnostic  Symptoms 

Lesions  in  the  upper  fourth  of  this  convolution  may  cause 
Jacksonian  epilepsy  commencing  in,  and  motor  paralysis 
of,  the  contralateral  leg.  Very  large  lesions  (hemorrhage, 
tumors,  etc.)  in  tliis  region  may  cause  also  paralysis  of  the 
homolateral  leg  in  a  lesser  degree. 


Lesions  in  the  middle  half  of  the  convolution  may  cause 
Jacksonian  epilepsy  commencing  in,  and  awkwardness  of  or 
loss  of  skill  or  complete  paralysis  of  the  contralateral  arm. 
Very  minute  lesions  in  the  upper  part  of  this  region  may 
affect  only  the  shoulder ;  in  the  lower  part,  only  the  hand. 

Lesions  in  the  lower  fourth  of  this  convolution  may  cause 
Jacksonian  epilepsy  commencing  in,  and  paralysis  of,  the 
contralateral  half  of  face  and  neck.  Very  minute  lesions  in 
the  upper  part  of  this  region  may  affect  only  the  eyes;  in 
the  lower  and  anterior  part,  the  tongue  and  larynx. 


The  base  of  the 
middle  left   fron- 
tal convolution. 


Small  lesions  in  this  area  may  cause  in  right-handed  per- 
sons, agraphia,  and  in  many  cases  Jacksonian  epilepsy, 
commencing  in  the  contralateral  arm. 


The  base  of  the  Small  lesions  in  this  area  may  cause,  in  right-handed  per- 
inferior  left  fron-  sons,  motor  aphasia,  and  in  many  cases  Jacksonian 
tal  convolution.  epilepsy,  commencing  in  the  right  side  of  the  face. 


f 


1305 

PARIETAL  LOBE 
Contains  the  centers 
for  cutaneous  and 
muscular  sensation. 
Many  lesions,  espe- 
cially tumor,  cause 
Jacksonian  epilepsy 
when  situated  in  the 
anterior  portion  of 
this  lobe ;  while 
lesions  in  posterior 
portion  may  cause 
epileptiform  con- 
vulsions.    (Fig.  15) 


The 

ascending 
parietal 
convo- 
lution. 


[^  Lesions   in    the   upper    fourth    of  this  convolution  may  cause 
some     blunting     of     cutaneous    sensibility,    and    especially 
I       astereognosis  in  contralateral  leg  and  foot. 

I  Lesions  in  the  middle  half  of  this  convolution  may  cause 
i  some  blunting  of  cutaneous  sensibility,  and  esi>ecially 
I       astereognosis  in  contralateral  arm  and  hand. 

I  Lesions  in  the  middle  half  of  this  convolution  may  cause 
j  some  blunting  of  cutaneous  sensibility,  and  especially 
L      astereognosis  in  contralateral  half  of  face. 


The  left  ang- 
ular gyrus. 

The  rest  of  the 
t  parietal  cortex. 


1306 

TEMPORAL  LOBE 

Contains,  on  the  left  side,  the  centers 
of    sensory  speech.        Lesions  may 
cause  epileptiform  con\'ulsions. 
(Fig.  15) 


Lesions  in  this  region  may  cause  loss  of  muscular  sense 
and  motor  ataxia  in  the  contralateral  arm  and  leg. 

Deep  lesions  in  this  region  in  right-handed  persons  may 
cause  alexia  and  hemianopia. 

Lesions  in  the  posterior  portion  of  the  left  superior  tem- 
poral convolution  in  right-handed  persons,  mav  cause 
sensory  aphasia  (psychic  deafness.) 


235 


LOCALIZING  SYMPTOMS  IN  LESIONS  OF  CEREBRAL  HEMISPHERES 

(Concluded) 


Seat  of  Lesion 


Diagnostic  Symptoms 


1307 

OCCIPITAL  LOBE 
Contains  the  centers 
of  sight.    Lesions 
may  cause  epilepti- 
form convTilsiohs. 
(Fig.   15) 


Neigh- 
borhood 
of 

calcarine 
fissure. 


I  Rest  of 
occipital 
(^  lobe. 


Lesions  in  this  area  cause  contralateral  homonymous  hemi- 
anopia.  A  lesion  limited  to  the  superior  lip  of  this  fissure 
causes  quadrantic  hemianopia  or  tetartanopia  of  the  con- 
tralateral lower  quadrants  of  field  of  vision.  A  lesion  lim- 
ited to  the  inferior  lip  of  this  fissure  causes  loss  of  contra- 
lateral upper  quadrants  of  the  field  of  vision. 

Lesions  in  this  area  may  cause  loss  of  power  of  recognition  of 
persons  and  things  (psychic  blindness). 


1308  Many  lesions  cause  a  mixutre  of  paralysis  and  convulsions  over  a  limited  area 
Cortical  Lesions.  which  in  some  cases  may  slowly  grow  larger.  The  intelligence  of  the  patient  is 
(Fig.   15)  always  more  or  less  impaired. 

1309  1-ocalized  lesions  in  the  white  substance  of  the  brain  (centrum  ovale)  may  involve 
Sub-Cortical  the  fibers  of  the  corona  radiata.  Such  lesions  when  lying  close  to  the  cortex  will 
Lesions.  cause  the  symptoms  characteristic  of  lesions  of  the  overl}'ing  cortex,  but  are  not 

quite  so  sharply  defined.     In  especial,  Jacksonian  epilepsy  and  mental  symptoms 
are  less  pnonounced  than  when  resulting  from  cortical  lesions. 


236 


CHART  XXII 


Cerebro-Spinal  Localization 


TOPICAL  DIAGNOSIS 


LOCALIZATION  OF  LESIONS  FROM  ANALYSIS  OF  SYMPTOMS 


ri314  _    1 

Sensation  alone,  in  all  its 
forms  is  lost  or  impaired 


1310 

PARALYSIS 
The  most  important 
of  all  localizing 
symptoms. 


1312 

The  reflexes  in  the  para- 
lysed area  are  abolished 
(except  in  1310  and  1329) 
A  lesion  of  the  periphera] 
neurons. 


1315 

Motion    alone    is    lost    oi 

impaired. 

1316 

Both    motion    and   sensa- 
tion are  lost  or  impaired  J 


I  See  Chart  XXII  a. 


1313 

The  reflexes  are    preseni 

(except  in  1357  and  1359) 

A    lesion    of    the    centra! 

neurons. 


1317 

Special     forms     of 
"  pheral  paralyses. 

1318 

Sensory    paralysis 

nant.     Little  or  no 

paralysis. 


peri-    See  Chart  XXII  b. 


domi- 
raotoi 


See  Chart  XXII  c. 


See  Chart  XXII  d. 


1319 

Motor  paralysis  domi- 
nant. Little  or  no  sen- 
sory paralysis. 

1320 

Both  motor  and   sensory  i 
>■  paralysis  well  marked. 

I  See  Chart  XXII  e. 

1311  I 

Jacksonian  Epilepsy,  together  with  other  symptoms  of  cerebral  disease.  j 

For  diseases  and  lesions  accompanied  by  motor  paralysis  see  469,  by  motor  spasm  see  570, 
by  ataxia  see  638,  by  tremor  see  639,  by  nystagmus  see  640,  by  fibrillation  see  641,  by  local  para- 
lysis see  636,  by  local  spasm  see  637,  by  disorders  of  speech  see  735,  by  disorders  of  gait  see  736, 
by  anesthesia  and  analgesia  see  811-15,  by  disorders  of  special  senses  808-10,  by  pain  see  931,  by 
vertigo  see  932,  by  mental  disorders  see  1036,  by  trophic  disorders  see  1121,  by  vaso-motor  dis- 
orders see  1130,  by  ganglionic  disorders  see  1129,  by  syphilis  see  1205,  by  abnormal  cerebrospinal 
fluid  see  1220. 


237 


CHART  XXIIa 

Cerebro-Spinal  Localization  Paralysis  with  Abolished  Reflexes 


R 
E 
F 
Ti 
E 
X 
E 
S 

A 
B 
O 

Ij 

I 

S 

E 
D 


1314 
Sensa- 
tion 
alone, 
in  all 
its 

forms, 
is  lost 
or  im- 
paired. 


I 


1315 
Motion 
alone 
is  lost 
or  im- 
paired. 


1310 
Both 
motion 
and 
sensa- 
tion 
are 
lest 
or  im- 
paired. 


TOPICAL  DIAGNOSIS 

LOCALIZATION   OF  LESION  FROM   ANALYSIS   OF  SYMPTOMS 
Diagnostic  Symptoms  and  Tests  Localization 


Area  of  anesthesia.  Onset 

etc.,  lies   within  ni-nte 

the  area   of  distri-  or  sub- 

bution  of  one  or  acute, 
more  nerves. 

Area  of  anesthesia.  Onset 

etc.,   lies  within  nciite 

the  area  of  distri-  nr 

bution  of  one  or  chronic. 
more  nerve   roots. 


Nerve   involved,    if  palpable,    is      Lesion  is  in  one  or  more  sen-     1321 


The  paralysis  is 
limited  to  mnsclM 
supplied   by    ouc 
or  more  nerves. 
(Figs.   19-21.) 


Tbn  paralysis  is 
limited   to  muscles 
supplied  by  one 
or  more  nerve 
roots.   (Figs.  19-21) 


Onset 
.icutp  or 
sub-acute. 
No  fever 
at  onset. 


Onset 
:<cute  or 
chr<)nic. 
May  be 
fever  at 
onset. 


tender  on  pressure.  No  symp- 
tom of  disease  of  central  organs 
usually,  unless  nuclei  are  af- 
fected. 


Nerves  involved,  if  palpable, 
are  not  tender.  May  be  symp- 
toms of  disease  of  central 
organs. 


Nerve  involved,  if  palpable,  is 
tender  on  iiressure.  No  symp- 
toms of  ilisease  of  central 
organs.  All  the  muscles  sup- 
plied by  the  neiTe  are  para- 
lysr-d,  usually. 

Nerve  involved,  if  palpable,  not 
tender.  May  be  symptoms  of 
disease  of  central  organs.  Often 
only  a  portion  of  the  muscles 
innervated  by  the  nucleus  are 
paralysed. 


U 
N 

1 
L 
A 
T 
E 
R 
A 


^  Motor  and  sensory 
j  paralysis  is  within  the 
1  area  of  distribution 
1  of  one  spinal  nerve. 

1  Motor  or  sensory 
paralysis  is  within  the 

I  area  of  distribution 
of  several  nerves  from 
one  plexus. 


Onset 

acute 

(ir  sub- 

:icute. 

Xo 

fever 

lit 

unset. 


Nerve  involved ; 
tender  on  pressure. 
No  symptoms  of 
disease  of  central 
organs. 


sory  cranial  nerves  or  nuclei  or 
sei/sory  end-organ ;  the  nerve 
affected  depending  upon  its 
anatomical  distribution  (822). 
(Figs.  19-21,  33,  aS). 

Lesion  is  in  corresponding  sen-     1322 
sory  nucleus  in  the  brain  stem, 
or  in  the  posterior  horn  of  spinal 
<'ord,  or  in  column  of  Burdach, 
or  in  posterior  nerve  root. 
(Figs.  19-21,  24-6). 

Lesion  is  in  one  or  more  motor  1323 
cranial  nerves,  or  a  mild  lesion 
of  mixed  spinal  nerves ;  the 
nerve  affected  is  the  nerve  sup- 
Iilying  the  paralvsed  muscles 
(4S9-<)3).  (Figs.  19-21,  .■«.  38). 

Lesion  is  in  corresponding  1324 
motor  nucleus  within  brain 
stem,  or  in  anterior  horn  of 
spinal  cord,  or  in  the  anterior 
nerve  root  (493-.5).(Figs.  19-21, 
24-6). 

Lesion     in     one     spinal     nerve     1325 
(4.S9L    (Pigs.  33.  .38). 


Lc-si.m    in    brachial    or    lumbar     1S26 
U'lexus   (490).     (Figs.  32.  as ). 


B 
1 
L 
A 
T 
K 
R 
A 


fNerves  involved  tender 
on  pressure.  No  symp- 
I  toms     of     disease     of 
I  central   organs. 


Muscles     show 
ness,     tenderness 
rapid   atrophy. 


weak-      Lesion  of  many  spinal    1327 
and       and      (rarely)      cranial 
nerves     also     (multiple 
neuritis)     (488). 


Motor 
and 

sensory 
paralysis 
extends 
over 
legs  or 
arms  or 
both, 
or  even 
more 
gener- 
ally. 


I  Inset 
.ii-ute 
or  sub- 
acute. 
.\Iav 
be 

fin'er 
at 
onset. 


.Nerves 
involved 
not  tender. 
There  are 
disturb- 
ances of 
organic 
reflexes 
and  other 
symptoms 
of  organic 
disease  of 
rentral 
organs. 


l.i'gs  alone 
are  para- 
!ys«l  anil 
exhibit 
trophi*' 
disturb- 
ances. 
.Anesthesia 
of   rectum 
and 
bladiier. 


(hvat  pain.     .May  be  deformity  Lesion   of 

of     lumbar     spines.      Symptoms  cauda 

less       symmetrical       and       bed-  equina 

sores      less     common      than     in  (487). 

lumbar      lesions.       Domain      of  (Fig.   29L 
anterior    crural    nerve    may    be 
normal   when   lesion   is   low. 


1338 


Little  pain.  May  be  de- 
fonnity  of  lower  dorsal 
spines.  Symptoms  sym- 
metrical. Red-sores  al- 
wa.vs  present.  No  por- 
tion of  legs  escapes. 


1329 


Both  legs  and  aims  are  p.iralyzed. 
There  are  trophic  disturbances  in  arms 
but  not  in  legs.  Reflexes  are  abolished 
ill   ;inii-:.   exaggerateii    in    legs.    ( .'i49-."il' I . 


Lesion   of   lum- 
bar enlargement 
of  spinal  cord 
(484-7). 
(Fig.  24-6). 


Lesion  of  cer-       133<l 
vical  enlargement 
of  spinal  cord 
I  Fig.    24-6). 


2.^9 


CHART  XXIIb 

Cerebro-Spinal  Localization 

Comprising  Numbers  1317  and  1331  to  1333  on  left  side  of  chart 
and  1334  to  1352  on  right  margin 


241 


1331 

DISTURBANCES      OP 
VISION.     (SOS). 


1317 

SPECIAL  FORMS  OF  PERI-    I  1332 

PHERAL  PARALYSIS.    -  PARALYSIS    OF   OCULAR 

REFLEXES     ABOLISHED    '      MUSCLES    (700). 

IN     PARALYSED     AREA,     ! 

EXCEPT  IN  1345.  | 


13;« 

FACIAL   PARALYSIS    (703). 


TOPICAL  DIAG] 
LOCALIZATION   OF   LESION   FROM 
PERIPHERAL    PARALYSIS    WITH 

DIAGNOSTIC    SYMPTOM 

r.linducss  of  eutire  field  of  vision  of  one  eye  is  present.  0 
lisht. 

Bitemporal  hemianopia  is  present.  The  outer  half  of  each 
l)resent.     Acromegaly  or  other  symptoms  of  a  lesion  ueai 

j  Xiisal  hemianopia  is  pi-esent.     The  inner  half  of  field  of  vi 
is  present.     May  be  symptoms  of  a  lesion  in  the  anterior 

Homonymous  hemianopia  is  present.  Identical  halves  (rig 
pupillary  reflex  is  present,  i.  e.,  reflex  is  absent  when  paral| 
toms  of  a  lesion  in  the  middle  fossa  of  the  cranium  mny  V 

.\11  muscles  of  one  eye  paralysed.     Eyeball  protruded  or  oti 

No  hemiplegia.     Other  cri 


All  muscles  supplied  by  third 
cranial  nerve  are  paralysed 
at  once. 


Paralysis  of  arm   and  leg 

Tremor  of  arm  and  leg  c 
motion,  causing  ataxia. 


I';uii;il   111-   pniyressive   paralysis  of  muscles  supplied  by  thii 

No  hemiplegia.     Other  era 


Pnr.ily.^is     of     external     rectus 
muscle. 


Hemiplegia  often  comliine 
power  of  conjugate  devi 
nerve  may  be  involved. 


r Lower  branch  of  facial  only,  or      Other  symptoms  of  disease 
mainly,  paral.vscd.  oration   never  present. 

Paralysis  of  arm  and  leg  c 


No  hemiplegia.     Chronic  cc 
tory  and  abduoens,  may 

Associated  with  unilateral 


Both  lower  and  upper  branches  -^'o  deafness  l)ut  hyperakus 
I  of  facial  nerve  equally  par-  J  Low  notes,  and  often  thi 
[     alysed.  1      taste.     At  times  absence 

Hyperakusis.     Loss  of  taste 


No  hyperakusis.     Loss  of  ta 


\o  hyperakusis.     No  loss  o 


!IS 

ALYSIS   OF  SYMPTOMS 

iOLISHED    REFLEXES 

IND   TESTS  LOCALIZATION 

nerve  is  atrophied.     Pupil  does  not  respond  to       Lesion  in  optic  nerve   (S97-S).  1334 

I  of  vision  is  blind.     Hemiopic  pupillary  reflex  is      T.esion  is  in  the  central  part  of  optic  chiasm   (362,  817,     1333 
!  sella  turcica   (1279)   may  be  found.  .SG4,  894). 

of  one  eye  is  blind.     Hemiopic  pupillary   reflex      Lesion  is  in  outer  mar^n  of  optic  chiasm   (3(;2.  817,  1336 

1  of  the  cranium  St55) . 

r  left)  of  each  field  of  vision  are  blind.    Hemiopic      Lesion  is  in  the  optic  tract  or  external  geniculate  body     1337 
half  of  retina  is  excited  by  light.     Other  symp-  of  opposite  side    (S62-!>.o). 

•esent. 

svidence  of  disease  within  orbit.  Lesion  is  within  the  orbit   (915).  1338 

nerves  paraivsed.  Lesion  of  3rd  cranial  nerve  truuk  or  nucleus   (TOO).  1339 

(Fig.  IS). 

jposite  side.  Lesion  involving  one  cms  cerebri    (676).  1340 

posite  side  present  at  rest  and  exaggerated  on       Lesion  of  red  nucleus  or  rubro-spinal  tract  on  same  side     1341 

as  motor  oculi  paralysis   (4.'^1,  G76). 

■anial   nerve  CTOO).  Lesion  of  3rd  cranial  nucleus,   in  whole     or  in   part  1342 

(700).    (Fig.  IS). 

nerves  paralysed,  especially  the  facial.  Lesion  of  fith  cranial  nerve  or  nucleus    (1346-7).  1343 

(Figs.  19,  20). 

ith   hemianesthesia    of   opposite    side.      Loss   of      Diffuse  lesion  of  Pons  Varolii    (53S,  885).     (Figs.  1344 

1  of  eyes  to  right  or  left.     Facial  or  auditory  19,  20). 

he  brain  present.    Electrical  reaction  of  degen-       Lesion  above  nucleus  of  facial  nerve  in  cerebral  hemi-       1345 
xes  present.  spheres  or  in  crura  cerebri.     (Figs.  15,  10). 

josite  side.     Often  abducens  paralysis.  Lesion  in  Pons  Varolii.      (Figs.  19,  20).  1346 

usually.  ■  Other  cranial  nerves,  especially  audi-       Lesion  of  nucleus  of  facial  nerve.      (Figs.  19,  20).  1347 

ffected. 

ess  anrl  vertigo  without  di.sease  of  the  ear.  Lesion  of  facial  nerve  trunk  at  liase  of  brain   (Fig.  19).     1348 

d  tinnitus  aiirium,  due  to  stapedius  paralysis.       Lesion  of  nerve  above  geniculate  ganglion    (928).  1349 

li  notes  also,  are  painful  to  hear.     No  loss  of  (Fig.  36). 

cretion  of  tears. 

aterior  two-thirds  of  tongue  of  same  side.  Lesion  of  facial  nerve  between  geniculate  ganglion  and       1350 

stapedius  branch.      (Fig.  36). 

1  anterior  two-thirds  of  tongue  of  same  side.  Lesion  of  facial  nerve  between  stapedius  and  chorda  1351 

tympani   branches.      (Fig.  36). 

e.     Tenderness  near  stylo-mastoid  foramen.  Lesion  of  facial  niTve  below  chorda  tvniiiani  branch.  1352 

(Fig.  36). 


CHART  XXIIc 

Cerebro-Spinal  Localization 


Comprising  Numbers  1318  and  1353  to  1359  on  left  side  of  Chart 
and  1360  to  1383  on  right  margin 


243 


TOPICAL  DIAGNOJ 

LOCALIZATION  OF   LESION  FROM   AN 

ANESTHESIA   WITH   EXAGGERAT 

DIAGNOSTIC    SYMPTOMS    AND    TESTS 

r  Marked  ataxia. 


r Limited  to  one  or  both  legs. 


Limited  to  one  arm. 


In  both  arms  and  both  legs. 


1353 

ANESTHESIA    with    or    with-   i 
out   ANALGESIA. 


lu  arm  and  log  of  same  side. 


Slight  ataxia. 
Slight   ataxia. 

Marked  ataxia. 
["Marked  ataxia. 
^  Slight  ataxia. 


In  arm  and  leg  of  one  side  and       Moderate  ataxia, 
in  other  side  of  face. 


In  arm,  leg  and  face  nf  same 
side. 


Slight   ataxia. 


318 

EN SORT 

ARALTSIS 

•OMINANT. 

JTTLE  OR 

fO  MOTOR 

ARALYSIS. 

ENDON 

.EFLEXES 

RESENT   OR 

iXAGGBRATED. 


1354 

ANALGESIA      with     THER- 
MIC ANESTHESIA,   but  little 
or     no     tactile     anesthesia,     is 
present.     DISSOCIATION  OF 
SENSATION. 


rt'sually   unilateral. 
In    one    or    both         | 
legs.  1 

t  Usually  bilateral. 


In    one    or    both 
arms. 


Usually    unilateral.       Leg    of 
.same  side  also  involved. 

Usually    bilateral.       Legs    of 
normal  sensibility. 


Anesthesia  marked,  bilateral.     Ma 
of  muscle  sense. 

Anesthesia  slight  and  most  market 
be  cerebral  symptoms,  Jacksonji 

.Anesthesia   slight,   most   marked 
other   cerebral    symptoms    (Jac 
paralysis. 

May  be  other  spinal  symptoms, 
in  arms  and  legs. 

May  be  other  spinal  symptoms, 
in  arm  and  leg. 

-\nesthesia  slight,   most   marked   i 
May  be  other  cerebral  symptoi 

May  be  paralysis  of  other  cranial 
of  the  eyeballs. 

No  Jacksonian  epilepsy.     Hernial 
Jacksonian  epilepsy  common.     N; 


No    trophic  disturbances.      No   ( 
ataxia. 

Trophic  disturbances  in  legs.     Oi 
usually  abolished,  especially  in 


No  trophic  disturbances.     Often  i 


Trophic  disturbances  in  arms.     ' 
especially  in  advanced  cases. 


In  arms,  or  legs, 
or  both. 


Rilateral     nsunlly,    marked 
ataxia. 


TJnilatpral,    slight    ataxia. 


1355 

HOMONYMOUS 

HEMIANOPIA. 


135C 

HOMONYMOUS 
TETARTANOPIA,   QUAD- 
R.VNT   HEMIANOPIA. 

1357 

PSYCHIC  BLINDNESS. 


1358 

SENSORY 

APHASIA. 


.\uditory. 


Visual. 


13.59 
ASTEREOGNOSIS. 


May   be   other   spinal    symptoms, 
paraplegia). 

llemianopia  and  anesthesia  usua 

.lacksonian   epilepsy   and   other  c 
thesia  present. 

Symptoms  of  Thrombosis  of  the  I 

In  contralateral  arm  and  leg  witl 

Idenlical  halves  of  each  field  of  vision   (right  or  left)   are  blind.     No  licmiopic  pupillary 
of  the  occipital  lobes  may  be  present. 


Identical  quadrants  of  each   field   nf  vision    (right  or  Icflt   arc  blind.     No  hemiopic  pupill 
anesthesia   or  other   paralysis.     May  be  other  cerebral  syinplimis  of  lesion  of  the  occipi 


Patient  is  not  blind,  but  cannot  recognize  things  by  sight,  though  lie  may  by  touch  or  hei 

Patient  is  not  deaf,  but  cannot  underetand  words  spoken  to  him,  allhou^li  he  nnderslaiid; 
memory  for  spoken  words. 

Patient  is  not  blind  but  cannot  umlerstand  written  words,  although   he  understands  them 
memory  for  written   words.     Alexia. 

Patient  is  not  anesthetic,  or  very  slightly  so,  but  cannot  recogniz  e  objects  by  the  sense 
sight. 


YSIS   OF   SYMPTOMS 

REFLEXES 

LOCALIZATION 

!  other  spinal  symptoms,  especially  loss      Lesion  in  one  or  both  posterior  columns  of  cord  in  dorsal  region.     Same     1360 

side  if  unilateral  (054,  7SC).    (Figs.  24-6). 

.  foot.     -Vlmost  always  unilateral.    May       Lesion  in  upper  one-fourth  of  posterioi-  central  convolution  in  contralateral     1361 
jpilepsy,  etc.  cerebral  cortex.     (Fig.  15). 

hand,   ascereognosis   marked.     May   be      l-Ksiou  in  middle  one-half  of  posterior  central  convolution  in  contralateral     1362 
aian   epilepsy).     Usually   some    motor  cerebral  cortex.     (Fig.  15). 

'Pnoea  common.     Loss  of  muscle  sense       Lesion  of  posterior  columns  of  cord  iu  cervical  region   (654,  786).  1363 

(Figs.  24-6). 

;pnoea  common.     Loss  of  muscle  sense       Lesion  of  posterior  column  of  cord  on  s;ime  side,  in  cervical  region    (654,     1364 

7S6).     (Figs.  ^-6). 

and  and  foot.     Astereognosis  marked.       Lesion  in  upper  three-fourths  of  posterior   central   convolution   of  contra-     1365 
especially  Jacksonian  epilepsy.  lateral  cerebral  cortex.     (Fig.  15). 

rves.     Paralysis  of  conjugate  deviation       Lesion  in  tegmentum  of  pons  Varolii  on  same  side  as  the  facial  anesthesia     1366 

(885).     (Fig.  20). 

»  common.  Lesion  of  posterior  part  of  internal  capsule  of  contralateral  hemisphere         1367 

(801,  1299).    (Fig.  17). 

mianopia.     Mental  deterioration.  Lesion  of  superior  parietal  lobule  of  contralateral  hemisphere   (657).  1368 

(Fig.  15). 

rbance   of   organic    reflexes.       Usually       Lesion  in  periphery  of  opposite  lateral  column  of  cord  in  dorsal  region         1369 

(1372).     (Figs.  24-0). 

c  reflexes  disordered.     Tendon  reflexes       Lesion  in  central  gray  matter  (anterior  commissure)   of  cord  in  lumbar  en-     1370 
•anced  cases.      (B^gs.  24-6).  largement.      In    central   gliosis    the   lesion   may   extend    upwards    to    the 

cervical  enlargement  and  involve  the  arms  secondarily   (840-2,  1372). 

a  without  loss  of  muscle  sense.  Lesion  in  periphery  of  the  opposite,  or  of  both,  lateral  columns  of  the  cord     1371 

in  the  cervical  region   (1373).      (Figs.  24-6). 

on  reflexes  usually  abolished  in  arms,       Lesion  in  central  gray  matter  (anterior  commissure)  of  the  cord  in  cervical     1372 

enlargement   (Syringomyelia)    (553,  693,  840-2,  1009,  1152-70-87,  1370). 
(Figs.  24-6). 

Iways   some    motor   paralysis    (spastic       Lesion  of  lateral  columns  of  cord  (053,  1212,  1309,  1371,  1400).  (Figs.  24-0).  1373 

present.     Other  cerebral  symptoms.  Lesion  of  posterior  part  of  contralateral  interu.il  capsule   (801).   (Fig.  17).     1374 

ral  symptoms   usually   present.     Ancs-       Lesion  of  inferior  parietal  lobule  of  contralateral  hemisphere    (0.^)7).  1375 

(Fig.  15). 

rior.  Inferior  Cerebellar  Artery  (1291).       Lesion   (softening)  of  the  lateral  half  of  the  pons   (1291).  1376 

.fness.  Lesion  of  ponto-cerehellar  angle  on  side  of  deafness   (428).  1377 

;.     Other  cerebral  syniplonis  of  lesions       Lesion   of  edges  of  calcarine  fissure   of  occipital  lohe,   or  of  fasciculus  of     137S 

Gratiolet  of  contralateral  cerebral  hemisphere  (302,  817,  890,  1307-19-21). 
(Fig.  10). 


:eflex.     No  hemi- 
jbes. 


Lower  quadrant  of  Lesion  of  upper  lip  of  contralateral  calcarine  tissure  (363,  817,  1307-19-21).    1379 
field   of  vision. 

Upper  quadrant  of  Lesion  of  lower  lip  of  contralateral  calcarine  fissure  (363,  817,  1307-19-21).     13S0 
field  of  vision.  (Fig.  10). 


He  has  forgotten  what  he  has  seen.       Lesion  of  cortex  of  occipital  lobe  of  left  cerebral  hemisphere    (232,  1307).     13S1 

(Fig.  16). 

n  when  he  sees  them  written.     Has  no       Lesion   of  cortex  or  subcortex  of  posterior  part  of  left  superior   temporal     13S2 

convolution  or  in  the  association  fil)ers  connecting  the  superior  temporal 
with   the  inferior  frontal  convolution    (222,  775).     (Fig.  15). 

u  he  hears  them  spoken.     He  has  no 

Subcortical  lesion  of  the  Angular  Gyrus   (777.  1403).  1382a 

)uch,  although  he  can  by  the  sense  of       Lesion  in  cortex  or  subcortex  of  the  posterior  central   convolution  of  con-     13S3 

tralateral  hemisphere   (229,  354).    (Fig.  l.T) 


4 


i 


CHART  XXIId 
Cerebro-Spinal  Localization 


Comprising  Numbers  1319  on  left  side  of  chart 
and  1384  to  1403  on  right  mars^in 


245 


TOPICAL  DIAGNO 

LOCALIZATION  OF  LESION  FROM  AI 

MOTOR  PARALYSIS   WITH   EXAGG 

DIAGNOSTIC    SYMPTOMS    AND    TESTS 

Limited    to   one   or    f  Symptoms  bilateral  usually.        May  be  otliei-  spinal  symptoms.     Often  at 

both   legs.    Organic   J  of  sensation  in  legs. 

reflexes   not   dis-        1 

ordered.  [Symptoms    unilateral    usually.    May   be    other   cerebral   symptoms,    especi 

b'psy. 


Limited      to       both 
arms  and  both  legs. 
Organic    reflexes 
not  disordered. 


'No  sensory  paralysis.     No  cerebral  symptoms.     Often  ataxia  and  dissoci 
arms  and  legs. 

Usually  some  sensory  paralysis.     Dysarthria  and  dysphagia.     Paralysis  ol 
ing  with  position  of  lesion. 


Limited  to  one  Occasionally  some  slight  sensory  pariil.vsis.     Jacksonian  tpilepsy  and  oth 

arm.  common. 


Limited  to  arm  and 
leg  of  same  side. 


Dissociation   of  sensation  and  ataxia  may   be  present.     Organic  reflexes 
cerebral  symptoms. 

Usually    some    sensory   symptoms.      Dysarthria    and    dysphagia    common, 
crania!  nerves  frequent. 


../..iLi.^  .Usually  some  st-asory  symptoms.    Jacksonian  epilepsy  and  other  sympton 

l.iTiiiti'<l  to  lownr  branch  of  facial  nerve.  i 


r.iV.)  I 

MOTOR   PARALYSIS 

DOMINANT.      LITTLE  |  r,imited   to  arm  and   lower  branch  of  facial   nerve 

OR  NO  SENSORY  -|      of  same  side. 

PARALYSIS.      TENDON  i 

RBFLEXBS  PRESENT  j  Limited   to  arm   and   leg  of  same   side  and   hypo-" 

OR   EXAOG-ERATED.  j      glossus  nerve  of  opposite  side. 

I  Limited   to   arm   and   leg  of  same   side  and   lower 
I      branch  of  facial  nerve  of  opposite  side. 


Jacksonian    epilepsy    and    other    .symptom, 
common.     Often  complicated  with  motoi 


Usually  some  sensory  symptoms.  Dysar 
I'aral.vsis  of  some  other  cranial  uervei 
aliduceus  paralysis. 


j  Liiiiitcd    to   arm    and   leg   of   same   side   and   motor       I'sually    some    sensory    syinptoms.      Parnl; 
I      "ciili   iici-ve  of  opposite  side.  ner\ os  common 


Limited   to  arm 
and  leg  and  lower 
branch  of  facial 
nerve  on  same  side. 


Symptoms  of  paralysis  rather 
than   of   irritation.     Not   pro- 

u'ressive. 


'Usuall.v  other  cerebral   symiiioms   present 
toms. 

Often   sensory  symptoms   present.     Paralj 
pressiou  on  opposite  side  of  face,  athctos 


Symptoms      of      irritation.  No  ob.iective  sensory  symptoms.     Often  mi 

Jacksonian     epilepsy. 


DYSARTHRIA  Paralysis  of  some  of  the  cranial  nerves  and  usually  of  arm  and  leg  also, 

and   DYSPHAGIA 


AGRAPHLV 


MOTOR 
APHASIA 

ATyRXIA 


Loss  of  power  of  writing,  although  arm  is  not  paralysed. 


Loss  of  power  of  speaking  some  or  all  words.     Limited  vocabulary.     Soui 
muscles  of  speech  not  paralysed. 

Inability  to  road,  although  patient  can  sec  and  can  spi>ak. 


.YSIS  OF  SYMPTOMS 

ATED   REFLEXES 

LOCALIZATION 

.  and  dissociation       Lesion  of  homolateral,  or  of  both  lateral,  columns  of  cord  in  dorsal  region  (1369    13S4 
1371-3).     (Figs.  25-7.) 

Jacksonian    epi-       Lesion   of  upper  part  of  anterior  central   convolution   of   contralateral    hemi-     1385 
sphere,  cortical  or  subcortical   (leg  center)-     (Fig.  15). 

1  of  sensation  in       Lesion  of  lateral  columns  of  the  cord  in  the  cervical  region  (525).  (Figs.  25-7.)    13SH! 

nial  nerves  vary-       Lesion  of  the  brain  stem   (involvement  of  pyramidal  tract  in  the  medulla,  pons     1387 
or  crura  cerebri).    (Figs.  19-22.) 

irebral  symptoms       Lesion  in  corte.x  or  subcortex  of  middle  one-half  of  anterior  centra!  convolution     1388 
of  contralateral  hemisphere  (arm  center).    (Fig.  15.) 

disordered.     No       Lesion  of  contralateral  lateral  column  of  cord  in  cervical  region.    (Figs.  25-7.)    1389 

iralysis    of   some       Lesion  in  the  brain  stem   (involving  the  pyramidal  tract).     (Figs.  19-22.)  1390 

cortical  disease.        Lesion  in  cortex  or  subcortex  of  upper  three-fourths  of  anterior  central  con-     1391 
volution  of  contralateral  hemisphere     (Fig.  15.) 

t  Lesion  in  cortex  or  subcortex  of  inferior  part  of  anterior  n'utral  convolution     139-'' 
of  contralateral  hemisphere   (face  center).    (Fig    15) 
cortical    disease     ! 

*^"'-  I  Lesioii  of  cortex  or  subcortex  of  lower  three-fourths  of  anterior  central  convo-     1393 

lution  of  contralateral  hemisphere   (arm  and  face  centers).     (Fig.  15.) 

and   dysphagia.     [  ^"'(Fil  "n")^"""  "''  ^^"^^  ^'"^^  "^  ^^^  hypoglossus  paralysis   (rare  condition).     1394 
imon,   especially   4 

I  Lesion  in  bridge  portion  of  pons  on  same  side  as  the  facial  paralysis.  (Fig.  20.)     1395 

)f   other   cranial       Lesion  in  pes  cruris  cerebri  on  same  side  as  the  motor  oculi  paralysis.   (Fig.  19.)  139i! 

■  sensory  symp-       Lesion  in  anterior  part  of  posterior  limb  of  internal  capsule  of  opposite  hemi-     1,'?97 
sphere.     (Fig.  17.) 

f  emotional   ex-       i.f^iou   in   posterior  part   of  optic  thalamus   and   corpus  striatum   of  opposite     139S 
"-•  hemisphere.     (Fig.  17.) 

^'^^^^-  I^esion    throughout   anterior    central    convolution    of    contralateral    hemisphere     1399 

(cortex  or  subcortex).     (Fig.  15.) 

Lesion  in  tegmentum  of  pons  or  me<lulla    (2S4-5.)     (Figs.  20-1.)  1400 

Cortical   or   subcortical    lesion   at   base   of   middle    frontal   convolution    of   left     1401 
cerebral  hemisphere  in  right  handed  person  (227-8.  779).    (Fig.  15.) 

n  be  made  and       C.rtical  or  subcortical  lesion   at   base   of  inferior  left   frontal   convolution   in     l-IO'' 
right  handed  person   (221,  774).     (Fig.  15.) 

Subcortical  lesion  of  left  angular  convolution  in  right  Ii.inded  person  or  involv-     140;H 
ing  the  association  fibers  connecting  the  inferior  frontal  convolution  with  the 
occipital  lobe  in  the  left  cerebral  hemisphere   (22S,  777).    (Fig   15) 


CHART  XXIIe 


Cerebro-Spinal  Localization 


TOPICAL  DIAGNOSIS 
LOCALIZATION  OF  LESION  FROM  ANALYSIS  OF  SYMPTOMS 
MOTOR  AND  SENSORY  PARALYSIS  WITH  EXAGGERATED  REFLEXES 


Diagnostic  Symptoms  and  Tests 


1320 
Both 
motor 
and 
sen- 
sory 
paraly- 
sis well 
marked. 
Reflexes 
present 
or  exag 
gerated, 
except 
in  1406. 


<'  Limited 
to  both 
legs. 


Limited 
to  both 
arms 
and  both 
I  legs. 


<'  Paralysis  severe.  No  ataxia.  Organic 
reflexes  much  disordered.  Some  of 
the  trunk  reflexes  are  lost.  Vertical 
extent  of  lesion  is  shown  by  the  ab- 
sence of  the  different  trunk  reflexes. 
Upper  limit  of  lesion  shown  by  the 
zone  of  hyperesthesia,  including  the 
anesthesia  above. 


Motor  paralysis  and  exaggerated  re- 
flexes in  one  leg;  anesthesia,  anal- 
gesia, and  thermic  anesthesia  in  the 
other  leg. 

Paralysis  not  so  extreme.  Marked 
ataxia.  Loss  of  muscle  sense.  Or- 
ganic reflexes  not  at  all,  or  slightly, 
disordered.  Trunk  reflexes  not  abol- 
ished. Knee-jerks  and  other  leg  re- 
flexes may  be  increased  or  abolished. 

No  involvement  of  cranial  nerves. 
Priapism.  Dyspnoea.  Very  dan- 
gerous, usually  fatal. 

Involvement  of  some  cranial  nerves. 
Dysarthria  and  dysphagia.  Very 
dangerous,  usually  fatal. 


Localization 

Transverse  lesion  of  spinal  1404 
cord  in  dorsal   region. 
(Myelitis).     (516-9,  829.) 


Unilateral     lesion     of     the  1405 
cord.       Brown  -  Sequard's 
Paralysis.     (432.) 


Lesion  both  in  lateral  and  1406 
posterior  columns  of  cord. 
(Ataxic  Paraplegia).  (526, 
660,  799).     (Figs.  25-7.) 


Transverse  lesion  of  spinal  1407 
cord  in  cervical  region. 
(512-5,  830).     (Figs.  25-6.) 

Lesions    on    both  sides  of  1408 
brain  stem   (medulla,  pons 
or    crura    cerebri,     accord- 
ing  to    cranial    nerves   in- 
volved).    (Figs.  19-21.) 


247 


TOPICAL  DIAGNOSIS— (Concluded) 
JACKSONIAN  EPILEPSY 


1311 
J 
A 
C 
K 
S 
0 
N 
I 
A 
N 

E 
P 
I 
L 
E 
P 
S 
Y 


(  Spasmodic    twitching    of    head    and    eyes    to    one     side. 
Tvvitcliing  may  remain  Hmited  to  these  muscles  or  may 
extend  to  other  muscles  of  face  and  neck  and  arm  and 
later   to   leg   of   same   side   or   may   finally   extend   to 
muscles  of  both  sides  of  bodv. 


Spasmodic  twitching  commences  in  one  side  of  face. 
Twitching  may  remain  limited  to  these  muscles  or  may 
extend  to  others  as  above. 


Spasmodic  twitching  in  hand  or  arm.  Twitcliing  may 
remain  limited  to  these  muscles  or  may  extend  to  face 
or  to  1^  or  to  both  simultaneously  of  same  side  and 
may  later  extend  to  muscles  of  other  side  of  body  also. 


Spasmodic  twitching  of  foot  or  leg.  Twitching  may  re- 
main limited  to  these  muscles,  or  may  extend  to  arm 
and  later  to  face  of  same  side  and  still  later  to  muscles 
of  the  other  side  of  body.     (Figs.  15.  16.) 

Spasmodic  twitching,  commencing  simultaneously,  in  arm 
and  face  of  same  side,  which  later  extends  to  muscles 
of  the  leg  of  the  same  side  and  still  later  to  muscles  of 
the  opposite  side  of  the  body. 

Spasmodic  twitching  commencing  in  arm  and  leg  of  same 
side,  which  may  later  extend  to  face  of  same  side  and 
may  later  extend  to  muscles  of  the  other  side  of  body. 


Lesion  in  or  near  base  of   1409 
middle   frontal   convolution 
of  contralateral  hemisphere. 
(Fig.  15.) 


Lesion    in    or    near    lower  1410 
quarter  of  the  central  con- 
vodutions    of     contralateral 
hemisphere.     (Fig.  15.) 

Lesion    in    or    near  middle  1411 
half    of    the    central     con- 
volutions   of    contralateral 
hemisphere.     (Fig.  15.) 

Lesion    in    or    near    upper  1412 
quarter    of    central    convo- 
lutions or   paracentral   lob- 
ule of  opposite  hemisphere. 

Lesion    near    and    equally  1413 
distant    from    motor    area 
of  face  and  arm  in  contra- 
lateral hemisphere.     (Fig.  15.) 

Lesion    near    and     equally  1414 
distant    from     motor    area 
of   arm   and   leg  in  contra- 
lateral hemisphere.     (Fig.  15.) 


Spasmodic  twitching  commencing  in   face  and  arm  and    Lesion    in    inferior  parietal   1415 
leg  of  same  side,  which  may  later  extend  to  muscles    lobule  of  contralateral 
of  opposite  side.  hemisphere.     (Fig.   15.) 


24S 


PLATES 


Fig.  15 

Schematic  representation  of  the  convex  surface  of  the    Ult    cfrcbial    hcinisiihcrc,    sliowing   the    motor   and 
scnsor>-  areas,  and  the  location  of  the  cortical   functions. 
See   1304-9-61-2-S-8-72-81-3-5-8-91-2-3-9,   1401-3-10-S. 


250 


Fig.  1 6 

Schematic  representation  of  tlic  median  surface  of  the  left  cerebral  hemisphere.     U.  L.  Q. 

qiuulrant    of    both    retinae.     I,.    L.  U.    —    Lower    left  ciuadrant  of  both  retinae. 
See  S56-7-60,   1307-7S-80,   T412. 


Upper  left 


FACIAL  \       ARM         LEG 

HYPOGLOSSAL 


Fig.  17 

Horizontal   Section  through   Right  Hemisphere  showing    the    principal     tracts    situated    in    the     Internal 
Capsule;   Kn,  Genu  of  Corpus   Callosum ;   F,   Fornix;   NC,   Caudate   Nucleus;    NL,   Lenticular   Nucleus;   OT, 
Optic  Thalamus,   Sp,  Splenium  of  Corpus  Callosum. 
See   1298-9,   1367-74-97-8. 

251 


Nucl.  Comiss.  post,  ot  ] 
I.TSC.  long,  dors,  i 

F.isc.  long   dors. 

Kk'nurll    Oculorn.-Kern 
•M   Ifv.ilor  palpcbr.ie. 

M.  obliquus  inferior 
M.  rectus  superior. 
M  rectus  internus. 
M  jectus  inferior. 


Fic.    iS 

Sclicmatic   reproeiil.iti'in   ui   ilu-   niulel   siliialcd  liciie.itli    the-    ilcior    of    the    Sylvian    aqueduct,  showing  the 
origin  of  the  posterior  commissure,  the  oculo-motor  and  trochlcaris  nerves,   as   well   as   the  nuclear  localization 
of  the  centers  for  tlie  individual  ocular  nuiscles   (after  Edinger.) 
See  692,  700,  818,  1332. 


252 


post. root 
P'-Cerv. 


root 
1     Cerv. 


Fig.  19 

Schematic  representation  of  brain  stem ;  showing  nuclei  and  nerve  roots. 
The  sensory  nuclei  and  nerve  roots  are  colored  red,  the  motor  blue. 
See  1 32 1 -4-39-48-66-87-90,  1408. 


253 


'<    <: 


•Deiter's  pucV 


-spinal  V 
-subst.gelat., 

anterolat.  tn 
(Gowers) 


superi 


or  oli 


Fig.  20 

Diagrammatic  transverse  section  through  the  pons  at  a  level  slightly  posterior  to  the  superficial  origin 

of  the  trigeminus- 
See  1292,  1321-4-43-7-66-9S,  1401-8. 


rned. raphe 
I  post  lonr.  fasc. 


-N  soli  tar. 


-V.  spiral  rt 

-subst.gelat. 

--N.am'big. 

dir.cerebel  tr 
(Flechsig) 

-  ant.lateral  tr. 
(Gowers) 

—  \nt  arcuate 
fibres 


Fig.  21 

Diagrammatic  transverse  section  through  the  medulla,  approximately  near  its  middle. 
See  1290-1,  1321-4-94,  1401-8. 


254 


col.  Go^l 

n. gracilis 
"Col.Biarda.c'h 
n.cuneatus 

-  "Spinal  V 

--subst  .gelat,. 
"  "TTit. arcuate fr. 

—  ant.Viorn 
-lemniscus 

—  olive 


Fig.  22 

Transverse  section  of  medulla  just  above  motor  decussation    and    just    above    line    of    junction    with  tlie  cord 

showinii;  tbe  sensor\'  decussation  and  the  topography  of  the  lowest  level  of  the  medulla. 
See   1290-1. 


Transverse  section  of  the  cord  just  at  the  line  of  iuncti  m  with  the  medulla.  sIiowuil;  the  motor  decuss'  tion  and 

the  topography  of  the  uppermost  level  of  the  cord. 
See  i2go-r. 


255 


Fic. 


DfAORAMMATIC    SECTION    OF    THE  SPINAL  CORD  TO  ILLUSTRATE 

ITS  PHYSIOLOGY 


Left   side   shows  situation  nf  lesions  causing 
disorders  of  motion  and  sensation. 


Right  side  -jIiou  s  situation  of  lesions  causing 
disorders  of  reflex  activity. 


Destructive  lesiniis  at  .M  or  E  cause  diminution,  slijjht  irritative  lesionr..  exaggeration,  of  motion. 
Destructive  lesions  at  S  cause  pennanent  anestliesia,  analgesia,  thermic  anesthesia  and  loss  of  muscle  sense. 
Destructive  lesions  at  T  cause  analgesia  and  thermic  anesthesia.  Destructive  lesions  at  P  cause  ataxia.  De- 
structive lesions  at  K  cause  loss  of  muscle  sense,  ataxia  and  anesthesia.  Irritative  lesions  at  S.  K,  T,  or  P, 
may  cause  exaggeration,  or  perversion,  or  both,  of  sensation.  Destructive  Ic^inns  at  D  cause  diminution,  and 
at  E,  exaggeration,  of  reHex  activity.  Slight  irritative  lesions  at  D  cause  exaggeration,  and  at  E  diminution, 
of  reflex  activity. 

Symptoms  of  lesions  at  .\I  are  described  in  252,  26,3,  41(5,  547-8,  791,  1 148-0,  12.VS  and  1324:  at  E  in  251,  254. 
-'56-  j^S-f*-  70Q-800.  IJ12  and  1384-6-9:  at  S  in  826;  at  T  in  1,169-71,1;  at  P  in  281,  642-5,1;  at  K  in  280,  654,  786, 
1322-60-.V4  and   I40(.i.     The  results  of  lesions  at  D  and  E  are  discussed  in  Chart  Va. 


Cervical   Enlargement 


Lumbar  b'nlargenient 


Fir,.   25 


LOCALIZATION  OF  NUCLEI  IN  THE  ANTERIOR     MORNS    OF    THE    SPINAL   CORD 

(After  Edinger  modified  from  Sano.) 


256 


Fig.  26 

A   SCHEMATIC   REPRESENTATION  OF  A  TRANSVERSE    SEt'TION    OF    THE   SPINAL   CORD. 
SE\'ER  \E  LEVELS  BEING  COMBINED  INTO  ONE 


DfvSCnNDING    Tr,.\CTS 

V.  S.  T.:^  vestibulo-spiiial   tract 
T.  S.  T.  =  tecto-spinal  tract 

D.  P.  T.=  direct  pyramidal   tract      /  corlico-spinal 
C.  P.  T.  =  crossed  pyramidal  tract  \  tract 

N.  S.  T.  =  rubro-spinal   and  thalanici  spinal   tracts 
S.  C.  ^  Schultze's  comma 


ASCENDJNC.    Tr.ACTS 

S.  T.  T,  =  spino-thalamic    tract 
A.  S.  C.  T.  =  anterior  spino-cerebellar  tract   \ 
P.  S.  C. 'T.  =  posterior  spino-cerebellar  tract  (Flecbsig's  tract) 
C.  C.  ^  Clark's  cokniin 


(Cowers'  tract) 


On  tbe  left  side  of  the  cord  are  represented  the  nerve  roots  and  tliose  bnndles  of  long  fibers  in  the  white 
columns  which  carry  impulses  downward  from  the  brain  to  the  spinal  cord,  and  on  the  right  side  are  represented 
these  bundles  of  long  fibers  in  the  white  columns  which  carry  impulses  upward  from  the  spinal  cord  or  spinal 
ganglia  to  the  brain.  It  hardly  needs  to  be  stated  that,  although  in  this  figure  these  long  bundles  of  fibers  are 
represented  on  one  side  only,  they  are  really  situated  symmetrically  on  each  side  of  the  cord.  The  short  fibers 
which  connect  ditiferent  levels  of  the  cord  together  are  not  represented  in  the  figure. 

Lesions  involving  the  pyramidal  tract  give  rise  to  a  spastic  paralysis  described  under  251,  254,  525-6, 
547,  660.  799-800,  1212  and  1.S84-6-9.  Lesions  involving  the  anterior  horns  give  rise  to  atrophic  paralysis,  the 
acute  forms  of  which  are  described  under  495,  791,  114S,  1233  and  132.J  :  while  the  chronic  forms  are  described 
under  547-8.  695,  1150  and  i,'^24.  Lesions  involving  the  posterior  horn  give  rise  to  symptoms  described  under 
r322.  Lesions  of  posterior  columns  give  rise  to  symptoms  described  under  785,  1302,  1347,  1350-1  and  1396. 
Lesions  of  the  spino-ccrebellar  tract  give  rise  to  symptoms  described  under  281  and  653.  Lesions  of  the  spino- 
thalamic tr;ict  and  of  the  anterior  commissure  of  the  giay  ma'ter  give  rise  to  symptoms  described  under  365, 
812  and  I3=;.t.  Lesions  of  the  whole  of  one  lateral  half  of  the  cord  give  rise  to  symptoms  described  under  442. 
509,  840,  (>8r  and  1405;  while  lesions  of  the  whole  transverse  section  of  tiie  cord  give  rise  to  symptoms  described 
under  485,  513-4-17-8,  520-T-50-3,  793-8,  827-30-1-8,  980,  1149,  1329-30  and  1404-7-  Lesions  of  posterior  spinal 
ganglion  give  rise  to  symptoms  described  imder  040-78, 


25; 


Fig.  2-/ 

Sclu'malic  representation  of  the  more  important   diseases  of   the   spinal   cord. 


Locomotor  Ataxia 
(lumbar  region) 


See    248,    .M5,    409-12-3-23,    661,  75g, 

7S5.    ^.ii}.    8gi,  .894,    912,  979,  988, 

io<T4.    1015,    1172.    1186,    1217  and 
I -'3 1 


See  525.  547-8,  670,  605.  800  iiml  1150 


Locomotor   Ataxia 
(cervical    region) 


Amyotrophic    Lateral    Sclerosis 


Acute  Stage        Chriinie  Stage 

.\ntcrior    Poliomyelitis 

Sec  (if)5,  791.  800,   1 148,  1150 

and  1233 


Descending  Degeneration   of 
Pvramidal   Tracts 


Syringomyelia 

See    f'()3,    S02-10-J,     1009,     115270-S7 

and   1370-2 


Mfilillld  c-<>r(lrnlh. 


Compression    Myelitis     with     the    ecmse- 

([nent  A^cendini,'  and   Descending 

Dejjcni'r.ations.     See  520,  7'AS. 

No  3  shows  the  point  of  the  compression 
with  the  whole  transverse  section  of  the  cord 
the  scat  of  an  inflammation. 

No.  I  shows  ascending  degeneration  of  the 
colnnnis  of  (loll,  nf  the  spino-thalamic  tracts, 
and  of  the  .intcrinr  ;nid  posterior  spino-cerc- 
hellar  tracts. 

No.  2,  close  to  the  lesion,  shows  in  addition 
a  slight  degeneration  of  the  cohmnis  of  Bnr- 
dach. 

Nos.  4-6  show  degeneration  of  the  crossed 
and  direct  pyramidal  tracts,  of  the  vestibulo- 
spinal, rubro-spinal,  and  thalamo-spinal  tracts 
and  of  Sclnilt/c's  comma. 

The  tipper  series  faces  uj)  and  the  lower 
down. 


UsJolla  lamballJ 


258 


SCHEMATIC  REPRESENTATION  OF  SOME  POINTS  IN  THE  PHYSIOLOGY  AND  PATHOLOGY 
OF  THE   SPINAL  CORD  AND  PERIPHERAL  NERVES 
Fic.  28.    Diagram  to  illustrate  the  mechanism  of  the  bladder  reflex. 


Fig.  28 


B  represents  the  bladder.  S  C  rep- 
resents the  reflex  centre,  with  its 
motor  and  sensory  neurons,  for  the 
sphincter  of  the  bladder,  which  is  ex- 
cited to  action  by  urine  in  the  neck 
of  the  bladder  or  in  the  prostatic  ure- 
thra. DC  represents  the  reflex  centre, 
with  its  motor  and  sensory  neurons, 
for  the  detrusor  of  the  bladder,  which 
is  excited  to  action  by  the  distention 
of  the  walls  of  the  bladder.  These 
two  reflexes  are  antagonistic  and  the 
sensory  surface  irritated  being  much 
larger  in  the  latter  (DC),  than  in 
the  former  (SC),  reflex,  the  de- 
trusor reflex  will  eventually  over- 
power the  sphincter  reflex  under 
normal  conditions.  S  T  represents 
the  sensory  tract  connecting  the  blad- 
der with  the  brain,  by  means  of 
which  the  individual  is  informed  as 
to  the  degree  of  fulness  of  the  blad- 
der. M  T  represents  the  motor  tract 
conecting  the  cerebral  with  the  spinal 
centre  by  means  of  which  the  indi- 
vidual can  inhibit  the  activity  of 
either  centre  ( up  to  a  certain  degree) 
and  increase  the  activity  of  the  an- 
tagonistic   centre. 

Fig.  29  illustrates  effects  of  lesions 
of   Cauda   equina. 


If  the  lesion  is  at  "A"  there  is  complete  motor  paralysis  of  both 
legs,  and  complete  anesthesia  of  thewhole  of  both  legs  and  of  the  perin- 
eum, buttocks,  scrotum  and  penis,  and  all  reflexes  of  the  legs  are 
abolished. 

If  the  lesion  is  at  "B"  there  is  complete  motor  paralysis  of  both  legs, 
except  tiie  flexors  of  the  thigh  and  the  extensors  of  the  leg,  and  complete 
anesthesia  of  the  perineum,  buttocks,  scrotum  and  penis,  and  of  the  pos- 
terior surface  of  the  thighs,  the  posterior  and  lateral  surfaces  of  the  legs, 
and  all  of  the  foot,  except  a  small  area  on  its  inner  surface.  All  the  re- 
flexes of  the  legs  except  the  knee-jerks  are  abolished. 

In  both  cases  the  muscles  atrophy,  there  is  no  zone  of  hyperesthesia 
above  the  anesthesia  and  the  bladder  and  rectum  show  a  motor  and  sen- 
sory paralysis. 

If  the  lesion  is  limited  to  the  conus  medullaris  there  is  a  paralysis  of 
the  rectum  and  bladder  and  an  anesthesia  of  the  penis,  scrotum,  perineum, 
one  inch  about  anus,  and  the  upper  two-thirds  of  the  posterior  surface  of 
the  thighs.      Otherwise  there  is  no  paralysis  of  motion  or  sensation. 


L.III. 


N.crur. 


D.XI. 


,  D.xn. 


L.II. 


m 


L.nr. 


l.IV. 


■'After  Fr.  S  c  11  u  1 :  J  e  -  K  5  st  e  r. 

Fig.  29 


■*k^ 


30 

Showing  the  innervation  of 
musales  through  more  than  one 
nerve  root,  so  that  the  destruction  of 
one  nerve  root  or  of  one  group  of 
nerve  cells  does  not  cause  a  com- 
plete and  permanent  paralysis. 


259 


Fig.  31 

A  diagram  showing  that  a  given 
sensation  area  of  the  skin  is  sup- 
plied by  filaments  from  several 
nerve  roots ;  so  that  division  of  one 
root  does  not  necessarily  produce 
total  anesthesia.  It  also  shows  the 
peripheral  overlapping;  so  that  the 
area  supplied  by  one  nerve  can  be 
almost  completely  supplied  by  neigh- 
boring nerves. 


Motor  and  Reflex  Functions  of  the  Spinal-Cord  Segments  (Modified 
AFTER   Starr  and  Edinger) 


Segment 


Cervical 


Muscles 


2-3 


i     r 


6-i 


17- 


8 

Dorsal     1 
2-12 
Lumbar 


'.! 


■3-^ 


Sacral 


1-2 


3-5 


Stemomastoid 

Trapezius 

Scaleni 

Small    rotators   of    head 

Diaphragm 

Lev.  ang.  scap. 

Rhomboids 

Spinati 

Deltoid 

Supinat.  long 

Biceps 

Supinat.    brev. 

Serrat.   mag. 

Pectoralis    (clav.) 

Teres   minor 

Pronators 

Brachialis   ant. 

Triceps 

Long  extensors  of  wrist  and 

fingers 
Pectoralis    (costal) 
Latiss.   dorsi 
Teres  maj. 

Long  flexors,  wrist  and  fingers 
Extensors  of  thumb 
Intrinsic    hand-muscles 
Dorsal  and  abdominal  muscles 
Abdominal    muscles 
Iliacus 
Psoas 
Sartorius 
Flexors   of  knee 
Quad,    femoris 
Int.  rotators  of  thigh 
Adductors  of  thigh 
Abductors   of  thigh 
Tibialis    ant. 
Calf-muscle,s 
Ex.  rotators  of  thigh 
Extensors  of  toes 
Peronei 

Long  flex,  of  toes 
Intrinsic  foot-muscles 
Perineal  muscles 


i;i 


Reflexes 


Dilatation  of  pupil  by  irri- 
tating side  of  neck,  4  cer- 
vical to  I  dorsal 

Scapular  reflexes,  5   C-I  D 
Supinat.  long.,  5  C 


Biceps,  5-6  C 
Triceps,  6  C 
Posterior   wrist,   6-8  C 
Scapulo-humeral,   7  C 

Anterior  wrist,  7-8  C 


Palmar,  7   C-I  D 

Epigastric,  4-7  D 

.Abdominal,  7-1 1  D 

Cremaster,    1-3  L 

Patellar,   2-4  L 
Bladder,   2-4  L 

Rectal,  4  L-2  S 
Gluteal,  4-5  L 


.Ankle-clonus.    I         c 
Achilles,  \  '"-^  * 

Plantar,   1-2  S 
Anal.  )         (. 

Virile,  f  •'  ■  ^ 


Fig.  32. 


260 


261 


■|1 


sir  T.  c•^o.Sp;^«.«T,..ct- 


Fig.  34 

LONG  MOTOR  PROJECTION  TRACTS 

For  lesions  involving  these  tracts  see  under  Fig.  26 


262 


Fic-  35 

LONG  SENSORY  PROJECTION  TRACTS 

For  lesions  involving  these  tracts  see  under  Fig.  26 


263 


Gasseriafv 

OtmyUon.' 


Vnerye- /sensory  root/  a/'^^ 


/ 


Tongue 


1  ^ICenicuiate  Canylu>nj 


Stylorrmw^tctd  fortimen 
-PosterwrAurCcular 


"^losso  pharyngeal 

FiC.  36 
DIAGRAM  OF  TRIGEMINAL,  FACIAL  AND  GLOSSOPHARYNGEAL     NERVES,     SHOWING 

COURSE  OF  TASTE  FIBRES. 
(After   Pun-es  Stewart) 


Optio  RadltUont 
Corpiu  Callotum 

Optic  ThaUmus 
Corp.  genic  exC 


Optic  IVsct 


Optic  Nerve 


iiual  Word  Centre 
S 


Auditory   Word-CeiiCre 


Kftriciculus  Uoranatu* 


Vocal  Word.C«ntre 


Lesion  at  i  produces  blindness  of  one  eye. 
Lesion  at  2  produces  bi-temporal  hemianopia. 
Lesion  at  3  produces  bi-nasal  hemianopia. 
Lesion  at  4  produces  R.  hemianopia  with  hemiopic 
pupil  reaction 


*^mu»-^ 


Fic.  2,7 
DIAGRAM  ILLUSTRATING  HEMIANOPIA 
(Modified   from  Vialet) 


Lesion  at  5  produces  R.  hemianopia  with  normal  pupil 

reaction. 
Lesion  at  6  produces  R.  hemianopia  with  normal  pupil 

reaction. 
Lesion  at  7  produces  psychic  blindness. 

j,„K"  ■"■- - Lesion  at  8  produces  Alexia. 

The  heavy  black  lines  represent  the  fibers  from  the  m.-iciila    lutea    in    each    retina,    the    point    of    central 

or  clearest  vision. 

264 


INDEX 


INDEX 


Roman  numerals  indicate  charts.    Arabic  numerals  indicate  marginal  numbers. 
Arabic  numerals  preceded  by  "p"  indicate  pages. 


Abasia :     See  Astasia 

Abdomen,     Boat-shaped     retraction     of,     XI, 

605 
Abdominal   reflex :  See  Umbilical  reflex 
Abdominal  spasm  or  cramp,  XII,  732 
Abducens     nucleus,     Conjugate     deviation    in 
lesions  near  the,  XIV,  885;  XXII,  1344 
paralysis.  XIV,  872;  XXII,  1343 
Abductor  laryngeal  paralysis,  XIII,  759 
Abscess,   Cerebral ;     See  cerebral 

Spinal :     See  spinal 
Abstraction,  p.  17 
Accommodation   reflex :      See   pupillary   reflex 

to   accommodation 
Achilles  reflex,  I,  62;  V,  3:8 
Acliillodj-nia,  XV,   looi 
Achondroplasia,  XVII,   1177 
Achromatopsia,  I,  13;  VI,  364;  XIV,  850 
Acromegaly.  I,  20;  XVII,  1197 
Acroparesthesia,  XVII,  1197 
Action,   p.    10 

Association,   p.   22 
Autochthonous,  p.  35 
Automatic,  p.  14,  35 
Involuntary,  p.  35 
Reflex:     See  Reflex 
Voluntary,  p.  14.  31 
Active  contracture,  I,  39;  IV,  264;  XI,  572. 
Acute  alcoholic  mania.  XVI,  1 109-12 

anterior   poliomyelitis :      See    poliomyelitis 
apoplectiform      polioencephalitis     inferior, 
X.  534-44 
superior,   X.   534-43;    XVI,    1046-7-8 
ascending  paralysis,  II,   170;   X,  482 
ataxia :      See   ataxia 
atrophic   paralysis  :      See   poliomyelitis 
bulbar    paralysis,    IX,    424;   X,   534-43-4; 

XVI,   1046-7-8 
delirium,  XVI,  iiii 
encephalitis,   multiple,   XVI,    1046-7-8 
Adams-Stokes'  disease,  XI,  58;  XVI,  1060 

phenomenon,  IX,  426 
Adiadocokinesia,  IV,  288 
Adiposis  dolorosa,  XV,  1012 ;  XVII,  117S 
Adiposogenital   dystrophy,   XVII,   1176;   XXI, 

1302 
Adolescent  insanity,  XVI,   1098 
Adrenalin,    Action    upon    nervous    system  of, 

p.  21 
Aesthesiometer,   L   48 
African   lethargy,   II.   142;   XVI,   1055 
Age  in  nervous   diseases,   II,  86 
Ageusia,  p.  10;  VI.  357;  XIV,  810 
Tests  for,  I,   17 


Agitated  dementia,  XVI,  I  IDS 

melancholia,  XVI,  1115 
Agnosia,  p.  17,  III,  221 
Agoraphobia,  III,  235;  XVI,  1074 
Agraphia,  p.  35;  III,  228;  XIII,  779-8o;  XXII, 
1401 

localization  of,  XXI,  1304;  XXII,  1401 
Agrypnia.  I,  18 
Akinesia,  IV,  241 

Akinesthesia,  I,  43;  VI,  352;  XIV,  813 
Albinism,   XII,   683 
Alcoholic    coma,    XVI,    1056 

convulsion,   XI,   576-85 

dementia,   XVI,    1103 

hallucinosis,    XVI,    1 112 

headache,  XV,  954 

intoxication,    XI,    585;     XII,     658-63-73; 
XIII,  767,  781 

mania,  acute,  XVI,  1 109-12 

neuritis    (or   paralysis),   X,   488 

tremor,  XII,  673 

vertigo,  XV,   1031 
Alcoholism,     I,    2;    II,    116-61-2;     XII,     658; 

XIII,  767-81 
Alexia,  p.  35 :  HI,  229 ;  XIII,  777 

localization  of.  XXII,  1403 
Allocheiria,  VI,  377 
Alopecia.  XVII,  1161 
Altruism,  p.  28 
Amaurosis,    VI,    358 

Uremic,  XIV,  853 
Amaurotic  idiocy,  XVI,  1087 
Amblyopia,  VI,  359;   XII,  682 

Hysterical,    XIV,    855 
Ambulatory  automatism,   XVI,   1061-71-3 
Amentia,  p.  28;  III,  211 

Diseases  causing,   XVI,   1078 
Amnesia,  I,  6;  III,  220;  XIII,  739-72 

Retroactive,   XIII,   772:    XVI,    1102 

Retrograde,   XIII,   772 
Amyl  nitrite  poisoning,  XIV,  845 
Amyotonia  congenita,  II,   105 ;   X,  483 
Amyotrophic     lateral    sclerosis,    X,    547;    XI, 

695:  XIII.  800:  XVII,  1 150 
Anakusia,  VI,  355;   XIV,  822 

Diseases   causing,    XIV,   822 

Tests   for.   I,    15 
Anal  reflex,  V,  307a 

Analgesia,  VI,  349 

Diseases   causing,   XIV,   811 

Localization  of  lesions  causing,  XXII,  1354 

Tests  for,  I,  50 


269 


INDEX 


Anarthria,  p.  35;  IV,  283;  XIII,  y^y-T^ 

Diseases  causing,  XIII.  Ji'j 

literalis,   XIII,   770 

spasmodica,   XIII,   771 
Anatomic  introduction,  p.  5 
Anemia,  cerebro-spinal  fluid  in,  XIX,  1244 

Optic   neuritis   in,   XIV,   902 

Vertigo  in,   XV.  1021-5 
Anemic  convulsion,  XI,  583 

lieadache,   XV,   950-3-9 
Anesthesia,  p.  6;  VI,  348;   XIV,  811 

Diseases  causing,   XIV,   811 

dolorosa.  VI,  374 

Glove  form  of,  VI,  348;  IX,  415 

Hysterical,  p.  7:  VI,  348;  IX,  415;  XIV, 
837;    XVI.    1076 

Laryngeal,    XIII,    757-63-4 

Localization    of    lesions    causing,     XXII, 

1353 

Stocking  form  of,  VI,  348 ;  IX,  415 

Tests  for,   I,  48 

Thermic,  VI,  350;   XIV,  8ri 
Tests  for,  I,  55 
Aneurism,   Cerebral,   X,   502 
Angina  pectoris,  XV.  984 
Anginal  crises,  IX,  423 
Angio-neurotic  oedema,  XVII,   i2or 

-paralytic    hemicrania,    XV,   950 

-sclerotic   dysbasia,   X,  555;   XVII,   1 199 

-spastic   hemicrania.   XV,  950 
hemiplegia,   X,   555 
Angular  gyrus,   Symptoms  of  lesions  of,  III, 

229;  Xin,  ^TJ■,  XXII,  1382a,  1403 
Anisocoria,  I.  24;  V,  341 
Ankle-clonus,   V,   317 

Tests  for,  I,  60 
Ankylosis,   Tests   for,   I,  z?- 
Anopsia,   VI,   358 
Anosmia,  VI,  356 

Tests  for,  I,  16 

Anterior    central    convolution:     See  localiza.- 
tion 

commissure   of   cord :      See   localization 

crural  neuralgia  or  neuritis,  XV,  997 

horn,  or  column  or  nerve  root:  See  spinal 
cord 
Apallesthesia,   VI,   353 

Tests  for,  I,  56 
Apathetic    dementia,   XVI,    1097,    1105 
Apathy,  III,  237 
Ape's  hand.  XII,  714 
Aphasia,  I,  6;  III,  222-3-4-5-6;   XIII,  739 

.'\uditory,    lU,   223;    XIII,    774 

Broca's  scheme  of,  XIII,  739 

Conduction,  p.  34;  XIII,  778 

Cortical    motor,   XIII,   774 
sensory,  XIII,  775-6 

Diseases   causing,   XIII,   739 

Marie's  theory  of,  XIII,  739 

Mixed,  III,  225;   XIII,  778 


Aphasia,    Motor,    III,    222;   XIII,  774;  XXII, 

1402 

Localization  of,  XXI,  1304;  XXII,  1402 
Optic,  III,  224;  XIH,  776;  XXII,  1357-81 
Sensory,    p.    17;    I,  6 ;    III.    223-4;   XIII. 

775-6-7 

Localization     of,     XXI,     1306;     XXII, 
135882 
Sub-cortical  motor,  XIII,  739 

sensory,   XIII,   739 
Trans-cortical  motor,  XIII,  778 

sensory,  XIII,  778 

Visual,  in,  224;  XIII,  ^^(, 

Wernicke's  theory  of,   XIII,  739 
Aphemia,  III,  222;  XIIL  774;  XXII,  1402 
Aphonia,  IV,  260;   XIII,  757-8,  60-1-2-3-4 

Hysterical,   XIII,   747-8-62 
Aphthongia.  XII,  729;  XIII,  771 
Apoplectiform     polioencephalitis     inferior,    II, 
118-69;  X,  495,  534-44;  XVI,  1046-7-8 
superior,  II,  118-69;  X.  495,  534-43;  XVI, 
1046-7-8 
Apoplexy,  II,   147,   189;  IX,  422;   X,  504;   XI, 
5&S;  XIV.  835-60-1;  XV.  1027;  XVI, 
T043-63-4-5-6 
Athetosis   after,   X,   503;   XI,  632 
Cerebral,    X.    504;    XI,    588;    XIV,    835; 

XVI,   1043-63-4 
Ingravescent,  XVI,  1043-63-4 
Meningeal,  X,  502-24;  XI,  588;  XVI,  1063 
Pontine.  XIII.  740 
Prodromata  of,  IX,  422 
Vertigo  from,  XV,   1027 
Apraxia.  p.  yj:  III,  231 ;  IV,  249-82;  XVI,  1106 
Association,   p.  },y 
Motor,  p.  yj 
Aran-Duchenne     type     of    muscular    atrophy, 
X,  548;    XII,  695;   XIII,  800;   XVII, 
1 1 50 
Arcus  senilis,  I,  24 

Argyll-Robertson's     pupillary    reflex,    V,     332; 
LX,  437 
Diseases  causing,   XIV,  891 
Arm-center,    Symptoms    of    lesion    of,   XXII, 
1 362-5-83-8-9- 1 -3-9,    141 1 
Paralysis  of,  XII.  708  to  13 
Spasm  of  muscles  of,  XII,  733 
Arsenical  neuritis,  II,  158;  X,  488 
.Arterial    disease    in    etiology    of    nervous    di- 
seases, II,  97 
cause  of  transient  motor  paralysis,  X,  558 
Arthralgia,  XV,   1000 
Arthritis    deformans,    XV,    976 
Arthropathy  of  tabes,   XVII,   1186 
Articulative  tics,  XIII,  771 
Asphyxia,  local,  XV,  ion;  XVI,  1059;  XVII, 

1 195 
Associated  movements,   IV,  276 
Association  of  ideas  and  memories,  p.  22 
Tests  for,  I,  5 
fibers,  p.  13 
reflexes,  p.   14.  31 


270 


INDEX 


Astasia  and  abasia,  IV,  287;  XII,  652;  XIII, 

795 
Astereognosis,  p.  17;  III,  230;  VI,  354;  XXII, 
-'35t^-83 
Tests  for,  I,  11 
Asthenic  tremor,  XII,  671 
Asthma,  XI,  616;  XVII,   1194 
Astrophobia,  III,  235 
Asynergia,  p.  36;   IV,  248 
Major,  IV,  281 
Minor,  IV,  282 
Ataxia,  p.  36 ;  I,  21-42 ;  IV,  248-80-1 ;  X,  488 ; 
XII,  638;  XVI,  1 104;  XXI,  1290-6 
Acute,  X,  488;  XII,  659-62 
Aural,  XII,  649 
Cerebellar,    p.    37 ;    I,    21 ;  IV,  281 ;  XII, 

642-50-69;   XXI,   1290-6,   i?04 
Cerebral,  p.  'S^ 
Diseases  causing,   XII,  638 
Dynamic,  p.  36;   IV,  280;  XII,  644 
Friedreich's  hereditary,  II,  104,   124;  XII, 

651-70-87;    XIII,    765-82 
Hysterical,  XII,  664 
Locomotor :     See  Tabes 
Marie's     hereditary     cerebellar,    II,     124; 

XII,   650-69;    XIII,    783 
Motor,  p.  36;  IV,  280;  X,  488;  XII,  644; 

XXI,   1290  to  97 
Ocular,  XII.  648 
Post-hem-plegic,    XII,   655 
Static,  p.  37 ;  IV,  281 ;  IX,  438 ;  XII,  642 
Vertigo  with.  XII,  648-91;  XV,  1015-20 
Ataxic  gait.  Diseases  causing,  XIII,  740 

paraplegia,  X,  526;  XII,  660;  XIII,  799 
Ateleiosis.   XVI,   1095 
Atheromatous     arteries.     Vertigo     from,     XV, 

1025 
Athetoid  spasm.  Diseases  causing,  XI,  574 
Athetosis,  p.  38;  I,  Zi\  IV,  271;  X.  501-4;  XI, 

574 
after  apoplexy,  X,  504 ;  XI,  632 
in   cerebral    palsy    of    childhood,   X,   501  ; 

XI,  631 
Congenital,  X,  501 ;   XI,  630 
Athlete,  Muscular  hypertrophy  in,  XVII.  1156 
Atonia,  I.  40;  IV,  240 
Atonic  paralysis.  I,  40;  IV,  252;  X,  472 
Atrophic  paralysis,  IV,  252;  X,  472-6-7,  S47-8 
Atrophies,    Degenerative,   X,   476 

Localized,  XVII,  1188 
Atrophy,  Arthritic,  XVII,   1127-53-86 

of  bone.  Diseases  causing,  X"VII,  113^79 
fat.  Diseases  causing,  XVII,  1 137 
joints,  XVII,   1 153 

muscles,  I,  41;  X,  476-7;  XVII,  1131 
skin.   Diseases   causing,   XVII,   1 133 
Attention,  p.  24 

Tests  for  power  of,  I,  5 
Attitudes  passionelles.  XI,  586;  XVI,  1076 
Attonita   melancholica,   XVI,   11 15 
Auctioneer's  cramp,  XII,  726 


Audition,  Cortical  center  of,  p.  8 
Auditory  aphasia.  III,  223;  XIII,  775 

nerve.  Deafness  in  atrophy  of,  XIV,  919 
Electrical   reaction  of,  VII,  403 
Lesions  of,  XIV,  920 
-orbicularis   reflex,   V,  314 
Aura  of  epilepsy,  IX,  420;  XIV,  849 
Glittering  scotom.ata  as,  XIV,  849 
of  migraine 

Glittering  scotomata  as,  XIV,  849 
Hemianopia  as,   XIV,  858 
Aural   ataxia,  XII,  649 
headache   XV,   953 

vertigo,  XII,  649-85;  XIV,  918;  XV,  1019 
Autochthonous  acts,  p.  35 
.Automatic  acts,  p.   14,  35 
Automatism.   Ill,  210;   XVI,   1038-9 
Ambulatory,   XVI,   1061-71-3 
Diseases  causing,  XVI,  1038-9 
Epileptic,  XI,  575;  XVI,  1061-73 
Spinal   reflex   of,  V,  327a 
Auto-suggestion    in    hysteria,    IX,    415;   XVI, 

1071-2-6 
Auto-toxic   coma,   XVI,    1069 

convulsion,  XI,  576-96 :  XVI,  1069 
Avellis'    syndrome,    IX,  449;   XII,  706;   XXI, 

l2go 
Awkwardness :     See  apraxia 
Axon,  p.  6 

Babinski  and  Nageotte's  bulbar  syndrome;  IX, 

427;  XXI,  1290 
Babinski's  associated  movements  of  trunk  and 
thigh.  IX.  436 
reflex,  V,  304,  328 
Tests  for,  I,  57 
Backache,   Diseases  causing,   XV,  935 
Barany's  test,  I,  79 
Barlow's  disease,  X,  495 
Basedow's   disease,   II,   132 ;    XII,  672 ;   XVII, 

"93 
Tests  for,  I.  20 
Bathyesthesia,   I,  43 

Bechterew's  reflex  :     See  dorsal  foot  reflex 
Bed  sores,  XVII,  1171 
Bell's  palsy,  XII,  703 

phenomenon,  IX,  434;  XII,  703 
Benedykt's    syndrome,    IX,   431;    XXI,      1293; 

XXII,   1341 
Beri-Beri  :     See  neuritis,  multiple 
Bewildered  mental  condition,  III,  207 
Biemacki's  sign,  IX,  439 
Binocular  diplopia,  V,  383;  XIV,  818 
Biot's  respiration,  IX,  425 
Bi-temporal    hemianopia,    VI,   362 ;    XIV,   817- 

64-94;   XXII,   1355 
Bladder  reflex,  V,  324 
Blepharospasm,  XI,  598,  615-6;  XII,  726 
Blindness.    V.    329;    VI.    358;  XIV.  853-4-5; 

XXII,    I33I-55-6-7 


271 


INDEX 


Blindness,  Color,  VI,  364 
Day,  VI,  360 

Diseases   causing,    XIV,   817 
Night,  VI,  361 
Psychic,  p.  17;  III,  224,  32;  XIII,  776-7; 

XXI,  1307;  XII,  1357 
Snow,  VI,  360;  XIV,  846 
Word,  III,  229;  Xni,  777 
Localization  of,   XXII,   1403 
Boat-shaped  retraction  of  abdomen,  XI,  605 
Bone,    atrophy    of,    Diseases    causing,    XVII, 
1139-79 
conduction.  Tests  for,  I,  15 
Failure  of  development  of,  XVII,   1138a 
Fragility   of,    XVII,    1141-85 
Hypertrophy  of,   Diseases  causing,   XVII, 

1 140,  1 180  to  84 
tissue,   trophic   lesions   of,    Diseases   caus- 
ing, XVII,  1 126 
Boston-Kocher  sign,  XVII,   1192 
Botulismus,   X,   542 
Brachycephaly,  I,  22 

Brachial    plexus,    Neuritis    or    injury    of,   IX, 
444-5 ;  X,  490 
Paralysis   of,    IX,   444-5;    X,   490;    XXII, 

1326 
Spasm  or  cramp  of,  XII,  733 
Symptoms  of  lesions  of,  XXII,  1326 
Bradycardia,  XII.  728 
Brain,  congenitally  defective,  p.  29 
puncture,   I,   75 
stem,  definition  of,  IX,  460 

Lesions  of,  U,  147-89;  X,  534  to  46;  XII, 
656:  XIV,  832;  XV,  1017;  XXI,  1290 
to    97;    XXII,   1321  to  4,   1387-90-4-6, 
1400-8 
Localization :      See   localization 
Tumor  of,  X,  535-7-9-4' ;  XII,  656 
Vertigo  in  lesions  of.  XV,  1017 
Bright's  Disease,  Optic  neuritis  in,  XIV,  899 
Brissaud's  lefiex,  V,  303 
Bristow's  syndrome,  IX,  452;  XXI,  1300 
Broca's  scheme  of  aphasia,  XIII,  739 
Brown-Sequard's  paralysis,  IX,  432;   X,  509; 
XIV,  844;  XV,  982;  XX,  1276;  XXII, 

1405 
Brudzinski's  leg  sign,   IX,   447 

neck  sign,  IX,  446 
Brun's  syndrome,  IX,  453 
Bulbar  paralysis,  IX,  424;  X,  544-6;  XII,  694; 
XIII,  759-64;   XVII,   1 151 
Acute,  X,  544 
Chronic    progressive,    X,    546;  XII,  69)4: 

XVII,   1 151 
Pseudo-.  X,  554 
Symptoms  of,  IX,  424 
Burdach's    column    and   nucleus:     See  spinal 
cord 


Caisson  disease,  X,  521 
Calcanodynia,  XV,  1002 

Calcarine  fissure.  Symptoms  of  lesions  of,  VI, 
364;    XIV,   850-6-7-9-60;    XXII,    1378 
to  80 
Caloric  reaction,  I,  79;  XII,  685 
Cannabis  Indica  poisoning,  XIV,  845 
Capsule,    External :      See   external 

Internal :     See  internal 
Caput  obsticum  paralyticum,  XII,  705 

spasticum,    XII,    705-30 
Cardiac  disease,  Vertigo  from,  XV,  1024 
Caries  of  the  spine,  11,  122 
Case  taking,  I 

Casque  neurasthenique,   XV,  960 
Catalepsy,  XL  609;  XVI,  1098 
Cataract,   Diplopia  in,   XIV,  882 

operation,  Perversion  of  vision  after,  XIV, 
846-7 
Catatonia,   XVI,    iioo 

Cauda  equina,  Paralysis  of,  X,  487;  XII,  721 
Symptoms  of  lesions  of,  X,  487;  XII,  721; 
XV,   1007;   XXn,   1328 
Causalgia,   XV,   1003a 

Central    Convolution,    Anterior,    Symptoms   of 
lesions  of,  XXII,  1385-8-91-2-3-9,  1410- 
1-2 
Posterior,       Symptoms      of      lesions,     of 

XXII,    1361-2-5-83 
Motor  (cortico-spinalj   neurons,  IX,  461 
Diseases  of,  X.  473 
Location  of  lesions  of,  XXII,  1313 
Sensory   neurons,   IX,   463 
Centrifugal  neurons,  p.  9 
Centripetal  neurons,  p.  6 
Cephalagia :     See  headache 
Cerebellar  abscess,  XIV,  909 

artery,   posterior   inferior.   Thrombosis  of, 

XXL   1291 
ataxia,    p.    37;    IV,  281;   XII,    642-50-69; 
XXI,   1290  to  1304 
Diseases  causing,  XII,  638 
Marie's  hereditary,  II,  124;  XII,  650-69; 
XIII,  783 
fits,  XI,  607-8;   XXI,   1295 
nystagmus.  I,  24-31-80;  XXI,  1295 
peduncles.    Symptoms    of    lesions    of    the 

middle.  XXL  1296 
tract   (direct).  Lesion  of  the,     XII,     653; 

XX I L  1369-73 

tumor,  IV,  909 
Cerebellum,  Diseases  of  the,  VI,  392 ;  XI,  607- 
8;   XII,  647-69-86;   XIII,  783-4;   XV, 
1016;  XXL  1295 
Lesions  of  the,  XII,  647-69-86;  XIII,  783- 
4 
hemispheres,  XI,  607 
vermis,  XI,  608 
Localization  in  :     See  localization 
Physiology  of,  p.   12 


272 


INDEX 


Cerebral  abscess,  II,  153,  174,  184;     X,     508; 

XI,    578,    587;    XIV.   907;  XV,   961; 
XVI,  1049 

Cerebro-spinal  fluid  in,  VIII,  405 ;  XIX, 
1238 

Headache  in,   XV,  961-7 

activity.  Diseases  causing  weakened,  XVI, 
I 040- I 

anemia.  Vertigo  from,  XV,  1021-2-3-4-5 

aneurism,  X,  502 

ataxia,  p.  yj 

apoplexy:     See  apoplexy,  cerebral  hemor- 
rhage and  softening 

compression,  XVI,  1043 

concussion,   XVI,   1042 

congestion,   XV,  958-1026 

contusion,  XVI,  1043 

cortex.   Symptoms  of  lesion  of  the,   XXI 
1308 

Conjugate  deviation   of  the  eyeballs   in 
irritative  lesions  of,  XIV,  819 

cyst:     See  cerebral  tumor 

decompression,   XV,   961 

diplegia,  II,  117;  IV,  255;  X,  478,  501; 
XI,  577,  614-31 ;  XIII,  801 ;  XVI,  1051- 
88 

disease.  Nystagmus  in,  XII,  689 

edema,    Cerebro-spinal    fluid   in,    VIII 

embolism,    X,   505;    XIV,   835-60-1;    XVI, 
1065 

endarteritis.     Syphilitic,    II,    178;    XVIII, 
1207 

gumma,   isolated,   XVIII,   1206 

hemorrhage,  II,  147,  189;  X,  503;  XI,  588; 

XIV,  835-60-1    XVI,    1043-64 
Cerebro  spinal     fluid     in,     VIII,     405-6; 

XIX,   1242 
into  ventricles,  X,  504 
localization :     See   localization 
meningitis  :      See  meningitis,   cerebral 
palsy  of  childhood,   II,   117;  X,  501;   XI, 

577;  614-31;  XIII,  801;  XVI,  1051-88 
softening,  X,  505-6 ;  XIV,  835-60-1 ;  XVI, 

1043-65-6 
syphilis,    XV,    1033;    XVIII,    1205 
Cerebro-spinal    fluid    in,    VIII,    412-3-4; 

XIX,    1230-1-2 
thrombosis,  X,  506 ;  XIV,  835-60-1 ;  XVI, 

1066;   XVIII.   1207 
tumor,  II,  125,  152,  191 ;  X,  S07-35-7-9-4I ; 

XI,  578-87;  XIV,  836-52-9-62-4-5,  908; 

XV,  961;,  1033;  XVI,  1050 
Cerebro-spinal  fluid  in,  VIII,  405-12-3; 

XIX,   1237 
Coma  in,  XVI,  1050 
Headache  in,  XV,  961 
Optic  neuritis  in,  XIV,  908 
Perversion  of  vision  in,  XIV,  852-9-62- 

4-5 
Vertigo  from,  XV,  1033 


Cerebration,  Disturbances  of,  III.  200 

Diseases  causing  disorders  of,  XVI,  1036 

Tests  of  I,  3  to  II 
Cerebro-spinal  fluid,  p.  38;   I,  74;  VIII,  404; 
XIX.  1220 

Abnormal,  XIX,  1220 

in  abscess.  XIX,   1238 

Albumen  in,  VIII.  411 

in  anemia,  XIX,  1244 

Bacteria  in,  VIII,  409;  XIX,  1223-4 

Blood  in,  VIII,  406 

Butyric    acid    test    in,    VIII,    412;     XIX, 

122r-2 

Cellular    elements     in,     VIII,    409;     XIX, 

1223-4 
in  cerebro-spinal  meningitis,  XIX.   1226-33 
clear  with  coagulum,     VIII.     408;     XIX, 

1223-4 
Cloudy,    VIII,   407;    XIX,    1223 
Colloidal  gold  test  in,  VIII,  414 
Globulin   in.   VIII,  412;   XIX.   1221 
in  hemorrhage  in  spinal  membranes,  XIX, 

1240-2 
in  herpes  zoster,  XIX,   1235 
in  hydrocephalus,  VIII,  405;  XIX,  1239 
Leucocytosis  in,  VIII,  409;   XIX,   1223 
Lymphocytosis  in,  VIII,  409;  XIX,  1224 
in  meningitis,  VIII,  405-9- 10- 1 -2 ;  XI,  590; 

XVIII,    1208-9-13-4;   XIX.   1226-7-8-9-32 
Noguchi  test  in,  VIII,  412 
Nonne-Apelt  test  in,  VIII,  412 
Obtaining  of,  I,  74 
in  paresis,   VIII,  409-12-3-4;   XIX,   1230 

poliomyelitis,  VIII,  409-12;  X,  495;  XIX. 
1233 

purulent    meningitis,    XIX,    1227 
Red  or  reddish  color  of  the,  VIII,  406 
in  serous  meningitis,  XIX,   1241 

sporadic  purulent  meningitis,  XIX,  1227 
Sugar  in.  VIII,  410 

in  syphilis,  VIII,  409-12-3-4;  XVIII,  1206 
to   17;   XIX,   1230  to  32 

tabes,    VIII,    409-12-3-4;    XVIII,    1217; 
XIX,  1231 
Tension  of  the,  VIII,  405 
in  tumor  of  brain  or  spinal  cord,  VIII,  405- 
XIX,   1237 

typhus  fever,  XIX,   1236 

tuberculous  meningitis,  XIX,  i22»-9 

uremia,   XIX,   1243 
Wassermann  test  in,  VIII,  413 ;  XIX,  1224 
Cerebro-spinal   syphilis,   II,    108,   175     to     80; 

XVIII,   1214;    XIX,   1232 
Cervical  region  and  enlargement:     See  spinal 
cord 
rib,  Symptoms  of,  X,  557 ;  XVII,  1 143 
Disorders  of,  XVII,  1122 
sympathetic.  Irritation  of,  XVII,  1192 

Paralysis  of,  XVII,  1 191 
Cervico-brachial  neuralgia,  XV,  995 


273 


INDEX 


Charcot's   disease,   XVII,   1186 
Charcot-Marie-Tooth's    type    of    muscular    at- 
rophy, X,  496;  XII,  731 
Chasmus,  XII.  73i 
Cheyne- Stokes'     respiration,   I,  451   IX,     425; 

XII,  728;  XXI,  1290 
Chills,  XII,  680 
Choked  disc,  Diseases  causing,  X,  507-8;  XIV, 

892 
Chondrodystrophia  foetalis,  XVII,   1177 
Chorea,  I,  33;  II,  ii3>  ^^b;  IV,  272;  XI,  573 

Degenerative,  XI,  625 

Electrical,  XI,  597.  628 

Dubini's,   XI,  597.  628 

gravidarum,   XI,   622-3 

Habit,  IV,  274;  XI,  627 

Herai-,  IV,  272;  X,  510;  XI,  573,  622 

Hereditary,  II,   103;   XI,  624 

Huntington's,   II,    103;   XI,  624 

Hysterical,  XI,  629 

Infectious,  XI,  622-3 

Insaniens,  XI,  623 

major  or  magna,  IV,  273;  XI,  629 

minor,  IV,  272;  XI,  622 

mollis,  X,  510 

Post-hemiplegic,  X,  501 ;   XI,  629 

in  pregnancy,  XI,  622-3 

Pseudo-chorea,   XI,   573 

Rhythmical;    Xi,    629 

Senile,  XI,  625 

Sydenham's,  XI.  622 
Choreic  movements,  I,  33;   IV,  272 

paralysis,  X,  510 
Choreiform  spasms.  Diseases  causing,  IV,  372; 

XI,  573 
Chromatopsia,   Tests   for,   I,    13 
Chronic  atrophic  paralysis,  X,  548;  XII,  6SH- 
5;  XIII,  800;  XVII.  1150-1 

bulbar  paralysis,  X,  546;  XII,  694;  XIll, 
759-64;    XVII,    1 151 
Chvostek's  sign,  IX,  441 ;  XI,  612 
Cilio-spinal  center,  IX,  465;  XVII,  1191-2 

reflex,  V,  335 
Circular   insanity,   XVI,    1119 
Circulation,  Tests  for,  I,  45 
Circulatory  disturbances.  Perversion  of  vision 

in,  XIV.  848-9 
Claudication,     Intermittent,   II,   190;   X,     555; 

XVII,   1 199 
Claustrophobia,  III,  23S;  XVI,  1074 
Claustrum  and  external  capsule,  Symptoms  of 

lesions   of,   XXI,    1301 
Clavus,  XV,  951 
Claw-hand,  X.  547;  XII,  715 
Cleft   palate,   XIII,  75' 
Clitoridian  crises,   IX,  423 
Clonic  spasm,  IV,  246 

Diseases  causing,   XI,   571 
Clubbed  fingers  and  toes,  XVII,  I184 
Coal  gas  poisoning,  XVI,  1058 


Coceygodynia,  XV,  972 

Coffee  vertigo,  XV,   1031 

Cold  as  an  etiological  factor,  II,  100 

Colic,  Lead,  II,   159;   XV,  989 

Colloidal  gold  test    VIII,  414 

Color  blindness,  VI,  364 

fields,   inversion   of  and  interlacing  of,  I, 
14;   XIV,  851-2 

sense.  Tests  for,  I,  13 
Coma,  I,  3;  HI,  205;  XIII,  745;  XVI,  1037 

Alcoholic,  XVI,  1056 

from  cerebral   compression,   XVI,   1043 
concussion,   XVI,    1042 

Diabetic,  II,  194;  XVI,  1067 

Diseases  causing,  XVI,   1037 

Epileptic,  XI,  575 ;  XVI,  1061 

Hysterical,    XVI.    1071 

in  internal  hemorrhage,  XVI,  1059 

Laryngeal,   XVI,   1062a 

Narcotic,   XVI,    1057 

Pseudo-,  Diseases  causing,  XVI,  1038 

Toxic  and  auto-toxic.  XVI,  1069 

Uremic,  I,  103 ;  XVI,  1068 

vigil.   Ill,  206 
Common  paths,  p.  II 

Comprehension.  Tests  for  power  of,  I,  5 
Compression  of  brain  stem,  X,  535-7-9-41 

Cerebral,   XVI,    1043 

myelitis,  II,  122;  X,  520;  XIII,  798 

neuritis,  XV.  939 
Compulsory    acts    and    ideas,  p.  10;  I,    4;  III, 

218;   IV,  275;   XVI,   1098 
Concentration,    p.    24 

Concentric    limitation    of    field  of  vision,  IX, 
415;  XIV,  817,  868  to  71 ;  XVL  1076 
Concepts,  p.   16 

Concussion,  Cerebral,  XVI.  1042 
Conduction  of  pain.  Retardation  of.  I,  51  ;  VI, 
381 

of  motor  impulses,  p.  9 
sensory  impulses,  p.  6 
Confusional    insanity,    XVI.    1108 
Congenital   dislocation  of  the  hip,  XIII,  788 
Congenitally    defective   brain,    p.    29 
Congestive  headache.  XV,  958 

vertigo,  XV,   1026 
Conjugate  deviation  of  eyeballs.  Lesions  caus- 
ing, XIV.  819-85-7 
Conjunctival  reflex.  V,  312 

Tests  for,  I,  58 
Consanguineous  marriages  in  nervous  dise2ses, 

I,  2;  n,  81 
Conscience,  p.  23 
Consciousness,  p.  18 

Disturbances  of,  I,  3;  III,  201;  XVI,  1036 
Consensual  pupillary  reflex,  I,  25 ;  V,  329 
Constipation   headache,   XV,  953-6 
Continuous  paralysis.  Diseases  causing,  X,  470 
Contraction,  Fibrillary,  IV,  293;  XII,  641 


274 


INDEX 


Contracture,  Active,  I,  39;  IV,  264;  XI,  572 

Dupuytren's,    XI,   621 

Hysterical,   XI,   6i8 

Passive,  I,  38;  IV,  263 

Post-paraplegic,    X,    480,  516  to  520;  549 

Post-neuritic,    X,   621 

Post-paraplegic,   X,   480;   516  to  520;   S49 
to  52;  XI,  620;  XIII,  742 

Tests  for,  I,  38-9 
Contusion,  Cerebral,  XVI,  1043 
Conus    terminalis    of    spinal    cord.    Lesion  of 

XIV,  833 
Convergence,  Deficient  and  cycloplegia,  V,  331 
Conversation  in  diagnosis,  I 
Convulsions,    p.    35;    IV,    242-69;    XI,    57c- 1 ; 
Sec  epilepsy 

Alcoholic,  XI,  576-85 

Anemic,  XI,  583 

Auto-toxic,  XI,  576-96;  XVI,   1069-70 

Cerebellar,   XT,  607-8 

Diseases  causing,   XI,  571 

Epileptic,  IX,  420-1;   XI,  575;   XIV,  849; 
XV,   1028;   XVI,   1061-73-85,   1104 

Febrile  or  toxic,  XI,  595-6 

Hysterical,  IX,  415 ;  XI,  586 ;  XVI,  1076 

Lead,  X,  4941   XI,  576-84-5 

Location  of  lesions  causing,  XXII,  1311 

Narcotic,  XI,  585 

Strychnine,   XII,  613 

Toxic  or  febrile,  XI,  595-6 

Uremic,  XL  576-81 
Convulsive  tics,   IV,   267-70;   XI,   598  to  602, 

616;  Xn,  726 
Coordination,  p.  12 

Tests  for,  I,  42 
Coprolalia.  XVL  1098 

Cornea.  Diplopia,  astigmatism  and  monocular 
diplopia  in  irregularities  of  the,  XIV, 
8S^ 
Corneal  reflex,  I,  58;  V,  312 
Comet  player's  cramp,  XI,  615;   XII,  726 
Corpora   quadrigemina,    Localization   in :      See 

localization 
Corpus    callosum.    Symptoms    of    lesions    of, 
XXI,  1300 

Striatum,    Localization    in :      See    localiza- 
tion 
Cortical  lesions  :     See  localization 
Cortical   reflexes,  p.   12 
Cortico-rubral  tract,  The.  p.  9 
Cortico-pontile  tract,  The,  p.  9 
Cramp,  XI,  615-6:     See  also  spasm 
Cranial  asymmetry,  I,  22 

fontanel  les,  I.  22 

hyperostosis,  XVII,  1 181 

nerves :     See  nerves 

nuclei :     Sec  nuclei 

sutures,  I,  22 

tumors,  I.  22 
Cranium,  Localization  at  base  of:     See  locali- 
zation 


Creative  faculty,  p.  25 
Cremasteric  reflex,  V,  308 

Tests  for,   I,  57 
Cretinism,   XVI,    1092;   XVII,    1164 
Crico-arytenoid,  posterior.   Paralysis  of,   XIII, 

759 
Crico-thyroid.   Paralysis  of,  XIII,  757 
Criminals,  Habitual,  p.  28;  XVI,  1106 
Crises,  Tabetic,  IX,  423;  XV,  988;  XVI,  1062a 
Crossed  hemianesthesia,  VI,  348;  XXI,   1292 
paralysis,    IV,    256;    X,    537   to   42;    XV, 

1017;  XXI,  1290  to  3:     See  also  Brown- 

Sequard's  paralysis 
Croup,  Spasmodic,  XI,  616;  XII,  728 
Crura    cerebri,    Hemorrhage    or    softening  in, 

X,  536-53 

Localization  in :     See  localization 
Symptoms  of  lesions  of  th»,  X,  536-7-43; 
XII,  656-76;   XXI,   1293 
XXII,    1340-1-2-5-87-96,   997,   1408 
Crural  neuralgia,  XV,  997 

paralysis.   XII,  717;   XV,  997 
Cutaneous     lesions.     Diseases    causmg,    XVII, 
1 124 
reflex  acts,  I,  57 ;  V,  297 
sensibility,   p.   6 

tissue.   Atrophy   of,    XVII,    1 133 
Eruptions  of,   XVII,   1135 
Hypertrophy  of,  XVII,  1134 
trophic     lesion     of.     Diseases     causing, 

XVII,   1124 
ulcerations  of.   Diseases  causing,  XVII, 
1 136 
Cyanosis,  Local,  XV,   loii  ;  XVI,   1059;  VII, 

1 195.     See  also  Raynaud's  disease 
Cycloplegia,  V,  331 
Cyst,  Cerebral :     See  tumor 

Dazed  mental  condition.  III,  207 

Dead  fingers,  XVII,  1195:  See  also  Raynaud's 

disease 
Deaf-mutism,  XIII,  744 

Hysterical,  IV,  283;  XIII,  747;  XVI,  1076 
Deafness,  p.  8;  VI,  355;  XIV,  822 

Cortical  center  involved  in,  XFV,  924a 

Diseases   causing,   XIV,  822 

Hysterical,  XIV,  924 

Psychic,  p.   17;   III,  223,  233;   XIII,  775; 
XXI,  1306 

Tests  for,  I,   15 

Word.  Ill,  223-33;  XIII,  775 ;  XXL  1306 
Decompression.    Cerebral,    XV,    961 
Decubitus,  XVIII,  1171 
Deep  reflex  acts.  I.  60  to  68;  V,  299 

sensibility,   p,   6 

Tests  for,  I,  43 
Defectives,  p.  28;  XVI,  1095 
Defensive  reflex   (Babinski),  V,  328 
Degeneration,  Electrical  reaction  of,  VII,  397- 
8,  402 


27: 


INDEX 


Degenerative  atrophies,  X,  476 

Chorea,   XI,  625 
Deiter's  nucleus,  p.  12 

tract,  p.  9 
DeHberation,  p.  31 
Delirium,  p.  29;  III,  217;  XVI,  1080 

Acute  or  grave,   XVI,   iiii 

tremens.   XVI,   1103-9-12 
Delusional  insanity,  III,  215;  XIII,  746;  XVI, 
1081,   1113 

Diseases  causing,  XVI,  io8i 
Delusions,  p.  29;  I,  4;  HI,  215 

of  grandeur,   XVI,   1 106-16 
observation,    XVI,    TI16 
persecution,   XVI,   11 16 

in   hysteria,   IX,   415 

Systematized,  p.  29 
Dementia,    p.    28;    III,    212;  XIII,  773;  XVI, 
1079 

Agitated,  XVI,  1105 

Alcoholic,  XVI,  1 103 

Apathetic,  XVI,  1097.  iioi-S-7 

Diseases  causing,  XVI,   1079 

Epileptic,  XI,  575;   XVI,   1061,   1104 

Paralytic:     See   Paresis 

precox,  p.  29;  XVI,  1098 

Primary,   XVI,    1097 

Secondary,  XVI,  1105 

Senile,  XVI,  1107 

Terminal,    XVI,    1105 
Demoniacal  possession,  p.  28 
Dendrons,  p.  6 

Dercum's  disease,  XV,   1012;  XVII,   117S 
Dermographia,    I.    59;    V,  327;    XVII,     1 167, 

1200 
Deviation  of  the  eyeballs,  conjugate,  Diseases 
causing,   XIV,   819 

Secondary,  of  the  sound  eye,  I,  30;  XIV, 
818 
Tests   for,   I,   30 
Diabetes  mellitus.  Coma  in,  II,  194;  XVI,  1067 

Fat  atrophy  in,  XVII,   1174 

Optic  neuritis   in.   XIV,  900 

Perforating  ulcers  in,   XVII,   1172 
Diadocokinesia,   I,   37 
Diagnostic  charts,  Introduction  to,  p.  127 
Diaphragm,  Paralysis  of,  XII,  707 

Spasm   of,   XII,   72^ 
Digestive  disturbances.  Vertigo  in,  XV,  1023 

Perversion  of  vision  iru  XIV,  848 
Diphtheritic  paralysis,  X,  488;  XIII,  756-7 
Diplegia,  IV,  255 ;  X,  478,  501 ;  XII,  703 

Cerebral:     See  Cerebral 

Facial,  XII,  703 

Infantile;     See   infantile 
Diplopia,  I,  24,  29;  XIV,  818 

Binocular,  VI,  383;   XIV,  8r8 

Diseases  causing,  XIV,  818 

Hysterical,   XIV,   880 

Monocular,  VI,  384;  XIV,  818 

Tests  for,  I,  29 


Displacement  of  eyeball,  XIV,  879 

lens,  XIV,  883 

retina,   XIV,  883 

visual  axis,  I,  29;   XIV,  818 
Disseminated     myelitis     or     sclerosis:       See 

sclerosis 
Dissociation    of    personality.    III,    209 ;    XVl, 
'039 

sensation,   VI,  365 ;   XIV,  812 

Diseases  causing,  XIV,  812;  XXII,  1334 
Disuse,  Bone  atrophy  from,  XVII,  1 178 

Muscle  atrophy   from,   XVII,   115S 
Diver's  paralysis,   X,  521 
Dolicocephaly,  I,  22 
Dorsal   foot  reflex,   I,  63 ;   V,  321 
Double  persoriality.  III,  209;  XVI,   1039 
Diseases   causing,   XVI,    1039 

pupillary  opening,   XIV,  881 

sensation,   I,  54;   VI,  378 

vision :      See   diplopia 
Drug   habit,    I,    i,    2;    X,    482;    XII,    658,63; 
XIII,  767;   XV,   1031 

poisoning,   II,   165 

vertigo,  XV,   1031 
Drunkenness  in  nervous  diseases,  I,  2;  II,  116 
Dubini's  disease,  XI,  597,  628 
Dupuytren's   contraction,    XI,   621 
Dwarfism,  II,  109;  XVII,  1164-77 
Dynamometer,  Testing  with,  I,  34 
Dysarthria,  p.  35;  I,  8;  IV,  284;  XIII,  738 

Diseases  causing,   XIII,  738 

Localization     of     lesions     causing,     XXI. 
1299;  XXII,  1387-90-4-5,  1400 
Dysbasia    angio-sclerotica,    II,    190;    X,     555; 

XVII,   1 199 
Dyschromatopsia,   I,   XIV,  851-2 
Dysmasesis,  IV,  2S6;  X,  554 
Dysmetria,   IV,   248-89 
Dyspepsia,  Headache  in,  XV,  953 
Dysphagia,  IV,  285 

Localization  of,  XXII,  1387-90-4-5,  1400 
Dyspinelismus,   XXI,    1303 
Dystonia   lenticularis,   XII,  668 
Dystrophia     adiposogenitalis,      XVII,      1176; 

XXI,  1302 
Dystrophies,  Bone  tissue,  XVII,  11 26 

Cutaneous,  XVII,  1124 

Fatty  tissue,  XVII.   1125 

Joint,  XVII,  1127 

Muscular,  II,  107-28;  X,  477;   XIII,  787; 
XVn,  1123 

Ear  disease  as  cause  of  headache,  XV,  953 

Deformity   of,   XVI,    1078 

Hyperemia  of  inner,  XIV,  ga? 

Lesion  of,  XIV,  gi8  to  921-7 
Echolalia,  XVI,   1098,   iioo 
Echopraxia,    XVI,    1098,    1 100 
Eclampsia,  XI,  576;  XVI,  1062 
Edema  angio-neurotica,  XVII,  1201 

Localized,  of  scalp,  XVI,  1044 


276 


INDEX 


Edinger-Westphal  nucleus,  V,  329 

Effectors,  p.  II 

Ego,  The,  p.  26 

Egotism,  p.  26 

Elbow  reflex,  I,  64;  V,  322 

Electrical  chorea,  XI,  597,  628 

motor  points,  I,  70;  VII,  393;  Vllb 
reaction,  I,  70  to  yz\  VII,  393,  395a 
of  auditory  nerve,   VII,  403 

degeneration,   VII,   397-8,  402 
Diminished,  VII,  395 
Exaggerated,  VII,  396 
Formula     of     degenerated     nerve     and 

muscle,  VII,  397 
of  normal  nerve  and  muscle,  VII,  394 
of  muscles  and  nerves,  I,  70  to  Ti\  VII, 

393,   395a 
Myasthenic,  VII,  399 
Myotonic,   VII,   400 
Neuritic,  VII,  401 
Normal,  VII,  394 
Electricity  and  the  nervous  system,  p.  38 

in  examination  of  nervous  patients,  I,  70 
to   n,  VII 
Embolism,   Cerebral,   X,   505 ;   XIV,  835-60-1 ; 

XVI,   1065 
Emotions,  p.  21 
Emotional    insanity.    Diseases    causing,    XVI, 

1082 
Emotions,  Disturbances  of,  I,   I ;  III,  204 

Tests  for,  I,  7 
Emprosthotonos,  IV,  265 ;  XI,  590,  603 
Encephalitis,  XVI,   1046 

Acute  multiple,  X,  495,  543-4;  XVI,  1048 
Epidemic,  lethargic,  XII,  677;  XVI,  1047, 
1234 
Encephalomyelitis,  XII,  659 
Endarteritis,     cerebral,     sj-philitic,     II,     178; 
XVIII,  1207 :     See  softening 
Spinal,    syphilitic,    II,    175;    XVIII,    1211 : 

See  spinal  cord 
Syphilitica,  II,   178;   XVIII,  1207-II 
Endocrinopathies,  XVIIb 
End  organs,  p.  5 
Enophthalmos,  XVII,  1191 
Enteralgia,  XV,  989 
Epicritic  sensibility,  p.  7 
Epidemic     cerebro-spinal      meningitis:        See 

Ccrcbro-spinal  meningitis 
Epigastric  reflex,  V,  310 

Tests  for,  I,  57 
Epilepsy,  I,  2;  II,  iii-27-45a;  IX,  420;  XI,  575; 

XV,  1028;  XVI,  1061-73 
Amnesia  in,  XI,  575 

Aura  of,  IX,  420;  XIV,  849;  XVI,  1061-73 
Automatism  in,   XI,  575;   XVI,   1061-73 
Double  personality  in.  III,  209;   XI,  575; 

XVI,  1039 

Glittering  scotoma  as  sura  of,  XIV,  849 
Idiopathic,  XI,  575;   XVI,  1061-73 


Epilepsy,  Jacksonian,  IX,  421 ;  XI,  587-8,  602; 
XXI,  1304;  XXII,  1311 

Major  attack  of,  XI,  575;  XVI,  1061 

Media,   XI,  575 

Minor  attack  of,  XI,  575 ;  XVI,  1061 

Nocturnal,  XI,  575;  XVI,  1061 

Procursive,  XI,  575 

Psychic  equivalent  in,  XI,  575 

Rotatory,    XI,   575 

Spinal,  I,  60-1;  IX,  433;  X,  509-20;  XIV, 
839-40 

Symptomatic,  XI,  576-87-8-95-6 
Epileptic  aura,  IX,  420;  XIV,  849;  XVI,  1061- 
73 

coma,  XI,  575;   XVI,   1061-73 

convulsion,  IX,  420;  XI,  575;  XIV,  849; 
XV,   1028;   XVI,   1061-73-85,   1 104 

cry,  XI,  575;  XVI,   1061 

dementia,  XI,  575;  XVI,  1061,  1104 

idiocy,    XVI,    1083 

insanity,  XI,  575;  XVI,   1061-85,  1104 

state,  XVI,  1061 

vertigo,  XV,  1028 
Epileptiform  convulsion,   XI,  571 
Equilibrium,  Sense  of,  p.  8 
Erb's  juvenile  form  of  muscular  dystrophy,  X, 
499;  XIII,  787;  XVII,  1 154 

paralysis,  IX,  444;  X,  490 

sign,  IX,  442;  XI,  612 

syphilitic  lateral  sclerosis,  X,  525;  XVIII 

12X2  ' 

Erotic  excitement  in  dementia,  XVI,  1107 

Erroneous   personality.    III,   208 

Eruptions,  Cutaneous,  Diseases  causing,  XVII, 

1135 
Erythromelalgia,  XV,  loio;  XVII,  1198 
Erythropsia,   XIV,  846 
Essential    tremor,    XII,    681 
Ethics,  p.  23 

Etiology  of  nervous  diseases,  I,  i ;  II,  83 
Eulenberg's  disease,  II,  106;  IV,  265;  XI   611  • 

XVI,   II 57 
Eunuchismus,    Pituitary,    XVII,    1176;      XXI, 

1302 
Examination  of  patients 

Brain  puncture,   Id 

Electricity,   Id 

Inspection,  lb 

Laryngoscopy,   Id 

Lumbar  puncture.  Id 

Ophthalmoscopy,    Id 

Palpation,   Ic 

Percussion,   Ic 

Questioning,   la 

Thermometry,  Id 
Excessive  sweating,  XVII,  1203 
Excitability,   Nervous,  p.  6 
Excitation,  Maniacal,  XVI.  1 1 18 
Exhaustion    in   etiology   of   nervous    diseases, 
n,  95;  Xin,  761 

Vertigo  from,  XV,  1022 


27; 


INDEX 


Exophthalmic  goiter,  1,  20;  II,  132;  XII,  672; 
XVII,   1 193 

Extension  of  inflammation  in  etiology  of  nerv- 
ous diseases,  II,  90 

External  capsule,  Symptoms  of  lesions  of  the, 
XXI.  301 
rectus,  Paralysis  of  the.  XIV,  872 

Exudative  disorders.  Diseases  causing,  XVII, 

1145 
Eye  as  cause  of  headache,  XV,  Q43-53 
in  disease,  I,  24 

Secondary  deviation  of  sound  eye,  I,  3° 
Eyeball,  Conjugate  deviation  of,  XIV,  819 
Displacement  of  the,  XIV,  879 
Limitation  of   motion   of  the,   XII,   1700; 

XIV,  818 
Optic  atrophy   in   disease  of     the,     XIV, 

910-S 
Paralysis  of  external  rectus,  XIV,  872 
inferior  oblique,  XIV,  877 

rectus,   XIV,  875 
internal   rectus,   XIV,   873 
superior  oblique,   XIV,  876 
rectus,  XIV,  874 
Spasm  of  the  muscles  of,  XIV,  878 

Face  center,    Symptoms  of  lesions  of,   XXII, 

1329-3-5 
Facial  expression  in  disease,  I,  20 
diplegia,  XII,  703 
hemiatrophy,    XVII,    ii79 
hemihypertrophy,    XVII    1180 
monoplegia,    XII,    703 
nerve.   Localization   of   lesions   of,    XXII, 

1333-48  to  52 
nucleus.    Symptoms   of   lesions   of,    XXII, 

1333-45-7 
paralysis,  XII,  703;  XIII,  754;  XIV,  928; 

XXII,  1333 

spasm  or  cramp,  XII,  726 
Facio-scapulo-humeral   type   of   muscular   dis- 
trophy,  X,  487;  XIII,  7^7  ■•  XVII,  1 154 
False  image.  Position  of,  XIV,  818 
Family  gangrene,   XVII,    1 196 

history  of  nervous  patients,  I,  2 

myoclonus  epilepticus,  XI,  601 

periodic    paralysis,    X,    556 
Faradism  in  examination  of  nervous  patients, 

I,  70-2 ;  VII,  393 
Fatty  tissue,   Diseases  causing 

atrophy  of,  XVII,  1:37 

hypertrophy  of,   XVII,   11 38 

trophic  lesions  of,  XVII,  1125 
Fear,  III,  235 

Feeble-minded,  p.  28;  XVI,  1094 
Febrile  or  toxic  convulsion,  XI,  595-6 
Festinating  gait    (festination),   XI,  610;   XII, 

677;   XIII,  769,  804 
Fibrillary  contraction    (fibrillation),  IV,  293 

Diseases  causing,  XII.  641 


Field  of  vision.   Limitation   of  the,   IX,  415 ; 

XIV,  817-68-71 ;  XVI,  1076 
Diseases   causing,   XIV,   817 
Tests  for,  I,  14 

Fits,  I,  I :    See  also  convulsion  and  spasm 

Cerebellar,  XI,  607-8;  XXI,  1295 
Flaccid  paralysis,  IV,  252 

Diseases  causing,  X,  472 

Tests  for,  I,  34  to  41 
Foot  drop,  I,  21;  II,  159;   X,  488-94;     XIII, 

789-90;   XVI,   1063 
Formication,  VI,  375 

Formula  of  electrical  reaction  of  degeneration, 
VII,  397 

normal   electrical   reaction,  VII,  394 
Foul   Air  headache,  XV,  955 
Fourth  ventricle.   Vertigo   from   lesion  within, 

XV,  1018 

Foville's  paralysis,  IX,  454;  XXI,  1292 
Fragility  of  bone,   XVII,    1141-85 
Free  will,  p.  32 
Frenzy,  Maniacal,  XVI,   11 18 
Friedreich's    hereditary    ataxia,      II.      104-24; 
XII;  651-70-87;  XIII,  765-82 
paramyoclonus  multiplex,  XI,  600 
Froehlich's  syndrome,  XVII,  1176;  XXI,  1302 
Frontal  convolution.   Symptoms  of  lesions  of 
the  inferior.  XXII.   1402 
middle,  XXII,  1401-g 
headache,  XV,  953 

lobes.   Symptoms  of  lesions  of  the,  XIV, 
886;  XXI,  1304;  XXII,  1401-2 

Gait,  Diseases  causing  ataxic,  XIII,  740 
disorder  of,  XIII,  736 
in  disease,   I,  21  ;   XIII,  736 
Festinating,  XII,  610-77;  XIII,  769,  804 
High  stepping,  X,  488;     XII,     662,     720; 
XIII.  789-91;  XV.  1008;  XVII,  1147-8; 
XIX,    1233;    XXII,    1327 
Mowing,   XIII.   797 
Paralytic  and  flaccid,   XIII.  741 
Spastic,  XIII.  742 
Scissors,  X,  501 ;  XIII,  798  to  803 
Gallon's  whistle,   I,   15 
Galvanic  excitation  of  nerves  and  muscles,  I, 

yz;  VII,  393 
Galvanism  in  examination  of  nervous  patients, 

I,  71-2 
Ganglionic  disorders.  Diseases  causing,  XVII, 

1122-9-30 
Gangrene,  Family,  XVII,  Iig6 

Symmetrical,  XV,   loii;   XVII.   1195 
Gastralgia,  XV,  987 
Gastric  crises,   IX,  423 
General  appearance  in  disease,  I,  20 
General   paresis :     See  paresis 

sensation,  p.  g 
Cieniculate   bodies.    Lesions   of,    XIV,    862-93 ; 
XXII,  T337 


278 


INDEX 


Genital  neuralgia,   XV,  991 
Gerlier's  vertigo,  XV,  1032 
Gigantism,  II,  109;  XVII,   1183 
Girdle  pain,  VI,  374 

Diseases  causing,  XV,  976  to  82 
Glaucoma,  XIV,  868;  XV,  944 
Glioma,  II,  125 

Central,  X,  553 
Glittering  scotomata,  XIV,  849 
Globus  hystericus,  IX,  416;   XI,     586;     XVI, 

1076 
Glosso-pharyngeal  paralysis,  XII,  703a 

spasm  or  cramp,   XII,  727 
Glossy  skin,  I,  40;  XVII,  1160 
Glove  form  of  anesthesia,  VI,  348;  IX,  415 
Gluteal   paralysis,  XII,  719 

reflex,  V,  307 

Tests  for,  I,  57 
Gordon's  reflex,  V,  305 
Graefe's  symptom,  XII,  672;  XVII,  1192-3 
Grandeur,  Delusion  of,  XVI,  672;  XVII,  1192-3 
Grand  mal   (le),  XI,  575;  XVI,  1061 
Grasset  and  Gaussel's  phenomenon,  IX,  448 
Gratiolet,    Lesions    of   the  optic  fasciculus  of, 

XIV,  859-60;   XXII,    1378 
Graves'  disease,  I,  20;  II,  132;  XII,  672;  XVII, 

1 193 
Green  vision,  XIV,  847 
Gumma,  II,  175 

Isolated  cerebral,  XVIII,   1206 
Spinal.    XVIII,    1210 
Gustation,  Cortical  center  of.  p.  8;  XIV,  810 
Gustatory  sensations,  p.  8 

Habit,  p.  26,  32 

chorea,  IV,  274;  XI,  627 

spasm,  IV,  274;  XI,  627 
Habits,  Sensory,  p.  14 
Habitation  as  cause  of  nervous  diseases,  I,  2 ; 

II,  89 
Habitual  criminals,  p.  29;  XVI,  1096 
Hallucinations,  p.  30;   I,  4-20;   III,  213 
Hallucinatory  insanity,  Diseases  causing,  XVI, 

1080 
Hallucinosis,  Alcoholic,  XV,  112 
Hand,  Ape's,  XII,  714 

Claw,  X,  547;  XII,  71S 

Obstetrical,  XI,  612 

Paralysis  of  muscles  of,   XII,  714-6 

Trident  shaped,   XVII,   1177 
Haphalgesia,  VI,  380 
Hare's  eye,   XII,   703 
Head  in  disease.  The,  I,  22;  XVI,  1078 
Head's  researches  on  sensibility,  p.  6 
Headache,  I,  i  ;  XV,  934 

Alcoholic,  XV,  954 

Anemic,  XV,  950-3-9 

Aural,  XV,  953 

in  cerebellar  tumor,  XV,  962 

in  cerebral  abscess,  XV,  961-7 


Headache,  Congestive,  XV,  958 

Constipation,   XV,   953-6 

Diseases  causing,  XV,  934 

Dyspeptic,   XV,  953 

Foul  air,  XV,  955 

Frontal,   XV,  953 

High   blood-tension   causing,    XV,  958 

Hydrocephalic,  XV.  961 

Indurative,  XV,  964 

Infectious,   XV,   965 

Meningitic.  XV,  963-6 

Menstrual.   XV,  950 

Migraine,  XIV,  849-58;  XV,  950.  I029 
Vertigo  in.  XV,   1029 

Morphine.  XV,  954 
Vertigo  from,  XV,  1031 

Neurasthenic,  XV,  960 

Occipital,  XV,  949-53 

Ocular,  XV,  953 

Pachymeningitic.  XV.  963 

Pelvic.  XV,  953 

Rheumatic,  XV,  964 

Sinus   thrombosis  causing,   XV,  966 

Sunstroke  causing,   XV,  968 

Temporal,   XV.  953 

Toxic.  XV,  965 

Tumor  causing,  XV,  961 

Uremic,   XV,  957 

Vertex,  XV,  953 
Heatstroke    or    sunstroke,  XI,  589;  XV,  968; 

XVI,    1070 
Hearing,  p.  8;  I,   15;  HI,  223-33;  VI,  355-72- 
So;  XIII,  744-75;  XIV,  809-22;  XXII, 
1382 

Cortical  center  of.  p.  8;  XIV,  822;  XXII, 
1382 

Diseases  causing  disorders  of,  XIV,  809 

Loss  of,  XIV,  822 

Tests  for,  I,  15 
Hebephrenia.  XVI,  1099 
Heine-Medin's  disease,  X,  495 
Hematorrhachis,  X,  524;  XI,  606;  XV,  973 

Cerebro-spinal  fluid  in,  XIX,  1240 
Hemeralopia,  VI,  360 
Hemianesthesia  altemans,  or  crossed,  VI,  348; 

XXI,  1292 

dolorosa,   XIV,  837a;    XXI,    1298 

and  hemianalagesia,  VI,     348 ;     IX,     4IS ; 

XIV.  843;  XXI,  1290-3 
Hysterical.  VI,  348;  IX,  41S  :  XIV,  837 
Transference  of,  IX,  415;  XIV,  837 
Hemianopia,  VI,  362;  XIV,  817-58-63-90 
as  aura  of  migraine,  XIV,  858 
Bi-temporal,    VI,    362;    XIV,    817-64-94; 

XXII,  1335 

Diseases  causing,   XIV,  817 
Homonymous,  VI,   362;   XIV,  817,  59  to 

63-95;    XXI,    1298,   1307,   1337;    XXII, 

1355-78 

Diseases  causing,  IV,  817-90 


279 


INDEX 


Hemianopia.  Horizontal,  XIV,  866 

Localization   of,   XXI,    1298,   1307;   XXII, 

I 355-6 
Nasal,  VI,  362;  XIV,  8i;-65;  XXII,  1336 

Diseases  causing,  XIV,  817 
Quadrantic,    VI,    363;    XIV,    816,    856-7; 

XXI,   1307;   XXII,   1356 
Tests  for,  I,  14 
Hemiataxia,  XII,  653  to  57 
Hemiatrophy,  Facial,  XVII,  1179 
Hemicrania,   XV,  950 

angio-paralytica,  XV,  950 
spastica,  XV,  950 
Hemichorea,  IV,  272;  X,  510;  XI,  573,  622 
Hemichromatopsia,  VI,  364;  XIV,  850 
Hemihypertrophy,    Facial,    XVII,    1180 
Hemiopic  pupillary  reflex,  V,  334 
Diseases  causing,  XIV,  817-90 
Tests  for,  I,  26 
Hemiplegia,  I,  21;  IV,  254;  X,  478-9-81 

altemans,  or  crossed,  IV,  256;  X,  537  to 
42;  XV,  1017;  XXI,  1290  to  93 
Facial,  IV,  256;  XXI,  1292 
Hypoglossal.   IV,  256;   XXI,   1290-1 
Oculo-motor,  IV,  256;  XXI,  1293 
Angio-spastic.   X,   555 
Complete,   IV,   254;   XXI,   1299 
Diseases  causing,  X,  478-9-81 ;  534-41 ;  XII, 

653-5-6;   XXII,   1384-5-88  to  99 
Homolateral,  IV,  254;  XXI,  1299 
Hysterical,    XIII,    796 
Infantile:  See  cerebral  palsy  of  childhood 
Lacunar,  XVI.   1066 
Organic,  XIII,  797 
Partial,  IV,  254 

Spinal,  IX,  432;  X,  509;  XIV,  844;  XV, 
982;     XX,     1276:  See    also    Brown-Se- 
quard's   paralysis 
Hemorrhage  (or  softening),  in  brain  stem,  X, 
534;  XII,  656:  XIII,  749;  XIV,  832 
XII,  1290  tfi  f:;; 
Cerebral,    11,    i-<7-S9;    X,    503;    XI,    588 
XIV,  8.r=;-f.n-i   XVI,  1043-64 
Cerebro-spinal      fluid     in,    VIII,    405-6 

XIX,    1242 
into  ventricles,  X,  504 
internal,  Coma  in,  XVI,  1059 
Vertigo   in.   XV,   1023 
Meningeal    cerebral,    II,    147-89;  X,  502; 
XI,  588;  XVI,  1043-63 
Cerebro-spinal      fluid    in,    VIII,    405-6; 

XIX,   1241-2 
Spinal,  X,  524 
of  spinal  cord   (or  injury)   above  cervical 
enlargement,  X,  512;  XIV,  830 
in  cervical  enlargement,  X,  547 
dorsal   region,   X,   516 
lumbar  region,  X.  484 
in    cms    cerebri    (or    injury    of),  X,  S36; 
XH,  656;  XXI,   1293 
Medulla,  X,  540-4;  XHL  749;  XXI,  1290 
pons,  X,  5.38-43;  XIII,  749 


Hepatic  crises,  IX,  423 

Hereditary  ataxia,  II,   104-24;  XII,  651-69-70- 
87;   XIII.  765-82-3 
chorea :     See  chorea 
infantile  poliomyelitis,  X,  5483 
Heredity  in  nervous  diseases,  I,  2;  II,  81 
Herpes,  I,  40:  XI,  590;  XIV,  834 

zoster,  XV,  940-8;  XVII,  1166;  XIX,  1235 
Cerebro-spinal  fluid  in,  XIX,   1235 
Herpetic  ganglionitis  or  neuritis,  XV,  940-78 
Hiccough,   XII,  731 
High  blood-tension.  Headache  from,  XV,  958 

Vertigo  from,  XV,  1026 
High    stepping   gait,    X,    488;    XII,  662,    720; 
XIII,      789-91;      XV,     1008;     XVII, 
U47-8;  XIX,  1233;  XXII,  1327 
Hip,  Congenital   dislocation  of,  XIII,  788 
Hippus,  V,  336 
History  taking,  I,  i 
Homonymous    hemianopia :       See  hemianopia 

scotomata,  XIV,  867 
Homer's  syndrome,  IX,  455;  XVI,  1191 
Hunger,  p.  9 
Huntington's   hereditary   chorea,   II,    103 ;   XI, 

624 
Hydrocephalic  cry,  XI.  593 

idiocy,  II,  120;  XVI,  1084 
Hydrocephalus,  I,  22;  II,  120;  XIV,  905;  XV, 
961;    XVI,    1084 
Cerebro-spinal    fluid    in,  VIII,  405;    XIX, 

1239 
Headache  in,  XV,  961 
Optic  neuritis  in,  XIV,  905 
Hydrophobia,  II,  173;  XI,  604 
Hydrorrhoea  nasalis,  XXI,   1302 
Hypakusia,  VI,  355 ;  XIV,  823 
Hypalgesia,  VI,  349;  XIV,  81 1-2 
Hyperakusia,  VI,  372;  XIV,  823 
Hyperalgesia,  VI,  367 
Tests  for,  I,  50 
Thermic,  VI,  368 
Hyperemic  reflex,  V,  327;  XVII,  1200 
Hyperesthesia,  VI,  366;   XIV,  815 
Tests  for,  I,  48 
Thermic,  VI,  368 
Hypergeusia,  VI,  370 
Hyperhidrosis,  XVII,  1203 
Hyperkinesis,  IV,  242 
Hyperosmia,   VI,   369 
Hyperostosis  cranii,  XVII,   1181 
Hypertonia,  I,  39;  IV,  240;  X,  473 
Hypertonic  paralysis,  IV,  251 ;  X,  473 
Hypertonic       pulmonary       osteo-arthropathy, 

XVII,  1 184 
Hypertrophies,  Localized,  XVII,   1188 
Hypertrophy  of  bone,  Diseases  causing,  XVII, 
1 140 
of  fat.  Diseases  causing,  XVII,  1138 
muscle,  1.  40 

Diseases  causing,  XVII,   1132 
in  an  athletic,,  XVII,  1156 
skin.  Diseases  causing,  XVII,  1134 


280 


INDEX 


Hypesthesia,  VI,  348;  XIV,  811 

Thermic,  VI,  35° 
Hypnotism,  XVI,  1071 
Hypochondriasis,  III,  216;  XVI,  1075 
Hypogeusia,  VI,  357;  XIV,  810 
Hypoglossus  paralysis,  XII,  706;  XIII,  755 

spasm  or  cramp.  XII,  729 
Hypokinesis,    IV.    241 
Hyposmia,  VI,  356 

Hypotonia,  I,  39;  IV,  240;  X,  472,  483 
Hypotonic  paralysis,  IV,  252;  X,  472 
Hysteria,  I,  2;  II,  1 12-29-31-54-82;  IX,  415;  X, 
527;    XIV,   846-S1-70,  926;  XV,   951- 
71-2-6-7 

Auto-suggestion  in,  IX,  415 ;  XVI,  1071-2- 

Concentric  limitation  of  field  of  vision  in, 
IX,  415;  XIV,  870 

Perversion  of  vision  in,  XIV,  846-51 

Traumatic,  XVI,  1077 

Vertigo  from,  XV,  1034 
Hysterical   amblyopia,   XIV,  855 

anesthesia,  p.  7;  VI,  348;  IX,  415;  XIV, 
837;   XVI,   1076 
Tests  for,  L  48 

aphonia,  XIII,  747-8-62 

ataxia,  XII,  664 

backache,  XV,  971 

chorea,  XI,  629 

coma,  XVI,  1 071 

contracture,  X,  618 

convulsion,  IX,  415;  XI,  586;  XVI,  1076 

deafness.  XIV.  924 

delusions,  IX,  415 

diplopia,   XIV.  880 

hemianesthesia,    VI,    348;  IX,  415;  XIV, 
837;   XVI,  1076 

hemiplegia,  XIII,  796 

hyperakusia  and  parakusia,  XIV,  926 

joint,  XV,  1000 

monoplegia,  X,  527;  XIII.  796 

mutism,  IV,  283;  XIII,  747;  XVI,  1076 

neuralgia,  XV,  951-71 

paralysis    I,    21;    IX,    415;  X,  527;  XIII, 
747-862-96;  XIV,  880;  XVI,  1076 

spasm,  IV,  268;  IX,  415;  XI,  616-8;  XII, 
637;   XVI,  1076 

suggestion,  IX,  415;  XVI,  1071-2-6 

symptoms,  IX,  415 

tremor,  XII,  674 
Hystero-epilepsy,  XI,  586 
Hysterofrenic  areas,  IX,  418 
Hysterogenic  areas,  IX,  417 

Ictus,  X,  479 

laryngeal,  IX,  423 
Ideas,  p.  17.  23 

Idiocy,  p.  38;  II,  loi;  XIII,  743;  XVI,  1083-9 
Idioglossia,  XIII,  753 


Idiopathic  epilepsy,  XI,  575;  XVI,  1061-73 

idiocy,  XVI,  1083-9 

imbecility,  XVI,  1090-3 

muscular   dystrophy,   X,  498 

neuralgia,  XV,  937 
Idiots  savants,  XVI,  1091 
Illuminating  gas,  poisoning,  XVI,   1058 
Illusions,  p.  291 ;  III,  214 
Imagination,  p.  25 
Imbecility,  p.  28;  II,  loi  :  XVI,  1090 

mattoids,  XVI,  1095 

moral,  XVI,  1096 

morons,  XVI.  1095 
Imagination,  p.  25 
Immobile  eyeball,  X,  545 

pupil,  V.  333 ;  X.  545 
Indurative  headache,  XV,  964 
Infantile    diplegia,    II,    117;    X,  501;  XI,  577. 
631 ;  XII.  801 ;  XVI,  1051-88 

hemiplegia,  II,  1 17;  X,  501;  XI,  577,  631; 
XIII,  801;   XVI,   1051-88 

hereditary  family  poliomyelitis,  X,  548a 

paralysis:     See  poliomyelitis 
Infection,   XVI,    1095 
Infectious  chorea,  XI,  622-3 

headache,   XV,  9<^5 

nervous  diseases,  I,  i ;  II,  93 
Inferior    oblique    muscle.    Paralysis    of,  XIV, 

877 
rectus  muscle,  paralysis  of,  XIV,  875 
Inflammation  in  brain  stem,  X,  534-43-4;  XII, 

656  .  . 

Cerebral :     See  meningitis,  encephalitis  and 

abscess 
of  nerves:     See  neuritis 

spinal  cord:     See  spinal  cord 
Infra-maxillary  neuralgia  or  neuritis,  XV,  946 

-orbital   neuralgia  or  neuritis,  XV,  945 
Ingravescent  apoplexy,  XVI,   1063-6 
Inherited   nervous   diseases,   II,  84 

tendencies   to,   II,  85 
Inhibition,  p.  11 
Injury,  I,  I  ;  H,  136-46 

of  Cauda  equina,  X,  487 
brachial  plexus,  X,  490 
nerve,     X,    489-92;     XIV,    824;    XVII. 

1 146-7 
optic    nerve,    XIV,  904;  H.    147-89;  X, 

524;  XIX,   1242 
or  hemorrhage,  of  spinal  cord 
cervical  enlargement,  X,  549 
cervical  region,  X,  512 
dorsal  region,  X.  516 
lumbar  region,  X,  484 
Innervation  feelings,  p.  18 
Insanity,  p.  28;  I,  2;  II,  110-30-5S;  XVI,  1041 
Acquired,  p.  29 

Adolescent  or  juvenile,  XVI.  1098 
Alcoholic,  XVI.  H02-9-12 
Catatonic,  XVI.   iioo 


281 


INDEX 


Circular,   XVI,   1 1 19-20 

Confusional,  XVI.  1108 

Congenital,  p.  29 

Delusional,  III,  215;  XIII,  746;  XVI,  1081, 

1 1 13-4-5-6 
Dementia,  XVI,  1097.  1 103  to  07 
Dementia  precox,   XVI,   1098 
Emotional,  Diseases  causing,  XVI,  1082 
Epileptic,   XI,   575;   XVI,   1061-85,   II04 
Febrile  and   Post- febrile,  XVI,   11 10 
Hallucinatory,    XVI.    11 12 

Diseases  causing,  XVI,  1080 
Hebephrenic,  XVI.  1099 
Korsakow's  psychosis,  X,  488;  XVI,  1 102 
Maniacal,    XVI.    1 12-4-8-20 
Manic-depressive,  XVI,  1120 
Melancholic,  XVI,   III5-7 
Paranoia,  XVI,  11 16 
Pananoid,  XVI,  iioi 

Paresis,  p.  29,  II,  135-80;  VIII,  409-12-3-4; 
XI,  579;  XII,  675;  XIII,  766;  XIV,  897, 
013;    XVI,    1052,    1 106;    XVIII,    1216; 
XIX,   1230 
Post-epileptic,   XII,  575;   XVI,   1061 
Puerperal,  XVI,  mo 
Recurrent,  XVI,  1120 
Septic,  XVI,  mo 
Tests  for,  I,  4 
Toxic,  XVI,  mo 
Insolation,  XI,  589;  XV,  968;  XVI,  1070 
Insomnia,  I,  18 

Inspection  in  diagnosis  I,  20  to  43 
Insufficiency  of  ocular  muscles,  XII,  692;  XIV, 

818 
Intelligence,  p.  25 

Disturbances  of,  III,  202 
Tests  for,  I,  5 
Intention  tremor,   IV,  291  ;   XII,  645 

Diseases  causing,  XII,  645 
Intercostal  neuralgia,  XV,  977 
spasm  or  cramp,  XII,  732 
Interlacing  of  color  fields,  I,  14;  XIV,  851-2 
Intermittent   limping  or  claudication,   II,   190; 

X,  555;  XVII,  1 199 
Internal  capsule.  Symptoms  of  lesions  of,  XIV, 
861;   XXI,   1279;  XXII,  1367-74-97 
rectus  muscle.  Paralysis  of,  XIV,  873 
sensations,  p.  9 
Interscapular  reflex,  V,  311 

Tests  for,  I,  57 
Intoxication,  Alcoholic,  XI,  585;  XII,  658-63; 

XII,  767-81 
Inversion  of  color  fields,  I,  14;  XIV,  851-2 
Involuntary  motions,  p.  35 
Iridoplcgia,  V,  339 
Iritis,  I,  24 
Irritation     of    sympathetic    ganglia.     Diseases 

causing,   XVII,    1143 
Ischemic  reflex,  V,  326 

Island  of  Reil,  Symptoms  of  lesions  of,  XXI, 
i3or 


Jacksonian  epilepsy,  IX,  421 ;  XI,  587-8 

Location  of  lesions  causing,  XXI,  1304-5; 
XXII,  131 1 
Janet's  test,  I,  48;  IX,  415 
Jargon  speech.  III,  226;  XIII,  778 
Jaundice,  Yellow  vision  in,  XIV,  845 
Jaw,  Paralysis  of  muscles  of,  XII,  702 
reflex,  V,  323 

Tests  for,  I,  65 
Spasm  of  muscles  of,  XII,  725 
Jendrassik's    method  of  reflex    reinforcement, 

I.  68 
Joint  sense,  I,  43 
Joints,    Diseases    causing   trophic    lesions    of, 

XVII,  1 127 
Joy,  III,  236 
Juvenile  insanity,  XVI,  1098 

Kahler's  disease,   XVIII,   1209 
Kak-ke :  See  multiple  neuritis 
Kalmuck  idiots,  XVI,   109S 
Keratitis,  I,  24 
Kernig's  sign,  V,  320 

Tests  for,  I,  66 
Kinesthesia,  p.  7;  I,  43 

Tests  for,  I,  42-3 
Knee-clonus,   I,  61 

-jerk,  I,  61 ;  V,  319 
pendular,  I,  6i 
Tests  for,  I,  61 
Knowledge,   Tests   for  general,   I,   5 
Klumpke's  paralysis,  IX,  445 ;   X,  490 
Korsakow's  psychosis,  IX,  451;  X,  488;  XVI, 

1 102 
Kyphosis,  I,  23;  XVII,  1183 

Labyrinth    disease    and     labyrinthine    vertigo, 

XII,  649-85;  XIV,  918;  XV,  1019 
Labio-glosso-pharyngeal-laryngeal        paralysis, 

IX,  412;  X,  546;  XII,  694;  XIII,  759- 

64;  xvn,  I  IS  I 

Lacunar  hemiplegia,   XVI,   1066 

Lagophthalmos,  XII,  703 

Lalling,   XIII,  753 

Landouzy-Dejerine  type  of  muscular  atrophy, 

X,  497;  XVII,  HS4 
Landry's  paralysis,   II,   170 ;   X,  482 
Lang's  colloidal  gold  test,  VIII,  414 
Language,  Zone  of,  p.  35 
Laryngeal  crises,  IX,  423 ;  XVI,  1062a 

exhaustion,    XIII,    761 

Nerve,   Paralysis    of    superior,  XII,  704; 

xm,  757 

inferior    (Recurrens")     XII,    704;    XIII. 
7S8 
vertigo,  IX,  423;  XVI,  1062a 
Laryngismus  stridulus,  XI,  616;  XII,  728 
Laryngitis,  XIII,  760 

Laryngoscopy     in     examination     of     nervous 
patients,  I,  77 


282 


INDEX 


Larynx,  Anesthesia  of,  XIII,  757-63-4 
paralysis  of,  XII,  704;  XIII,  757-8 
spasm  of,  XII.  728;  XIII,  757-8 
Lasegue's  symptom,  IX,  419 
Lateral  column :     See  spinal   cord 
sclerosis,  X,  525-47;  XIII,  800 
Amyotrophic,   X,   547;   XII,  695;   XIII, 

800;  XVII,  I  ISO 
Erb's  syphilitic,  X,  525;  XVIII,  1212 
Lateropulsion,   XXI,   1292-5-6 
Lead  colic,  II,  159;  XV,  989 

convulsion,  X,  494;  XI,  576-84 

palsy,    II,    159;  X,  494;   XII,  716;    Xin, 

790;  XVI,   1053 
poisoning,  Optic  neuritis  in, 
Leg  center:     See   localization 

paralysis  of  muscles  of,  XII,  717-21 
spasm  of,  XII,  733 
Le  grand  mal  of  epilepsy,  XI,  575 ;  XVI,  1061 
Lemniscus,  Lesion  of,  causing  deafness,  XIV, 

922 
Lenticular  progressive  degeneration,  XII,  668 
Le  petit  mal  of  epilepsy,  XI,  575 ;  XVI,  1061 
Leontiasis  ossea,  XVII,  1181 
Leprous  neuritis,  II,   141;  XVII,  1169 
Lethargic   encephalitis,    XII,   677;   XVI,   1047; 

XIX,  1234 
Lethargy,  African,  II,  142;  XVI,   1055 
Leucoderma,  XVII,  1162 
Levator  palati.  Paralysis  of,  XIII,  756 
Limping,  Intermittent,  X,  555;  XVII,  1 199 
Lisping,  XIII,  753 

Little's   Disease :  See  Cerebral  palsy  of  child- 
hood 
Local  asphyxia.  XV,  loii  ;  XVI,  1059 

cyanosis,    XV,    roii;    XVI,    1059;  XVIL 

1 195 
paralysis,  IV,  259 ;  X,  481 ;  XII,  700  to  721 
spasms,  XI,  571-2;  XII,  637 
syncope,  XVII,  1195:     See  also  Raynaud's 
disease 
Localization,  p.  13;  XX,  XXI,  XXII 
at  base  of  cranium,   XXI,   1297 
by  Jacksonian  epilepsy,  XXII,   131 1 
by    paralysis,    motor    and    sensory,  XXII, 

1310 
Cerebellar,    XXI,    1295 

direct  tract,   XII,   1295 
hemispheres,  XI,  607 
peduncle   (middle),  XXI,   1296 
vermis,  XI,  608 
Cerebellum,  Symptoms  of  lesions  of,  XXI, 

1295 
Cerebral,  XXI,  1290  to  1309 

brain     stem,     X,     5,34-45 ;     XII,    656 ; 

XIV,  832;  XXI,  1200  to  97;  xxn. 

1321-4-87-90-4-6,   I 40 I -8 
abducens    nucleus,    XIV,  872;    XXII, 

1343-4-46-7 
corpora  quadrigemina,  XXI,  1294 


Localization,  crura  cerebri,  X,  536-7;  XII,  676; 

XII,   1293;  XXII,   1340-5-96,   1408 
dysarthria      and      dysphagia,      XXII, 

1387-90-4-5,    MOO 
facial  nucleus,  XXII,  1345-7 
fourth   ventricle,   XV,   1018 
ganglia  at  base,  XXI,  129  to  1303 
lemniscus,  XIV,  129  922 
medulla   oblongata,    X,    540-1-4;    XII, 

656;  XIII,  749;   XXI,   1290;   XXIL 

1387-94,   1400-8 
motor  cranial  nuclei,  XXII,  1324 
pons    Varolii,    X,  538-9-43;  XIV,  843- 

85;   XXI,   1292;   XXII,    1344-66-76- 

95,  1401-8  

ponto-cerebellar  angle,  XXII,  377 
red  nucleus,  XXI,  1293;  XXII,  1341 
rubrospinal  tract,  IX,  431;  XII,  676; 

XXI,  1293;  XXII,  1341 
sensory  cranial  nucleus,  XXII,  1343 
sixth  cranial  nucleus,  XXII,   1343 

hemispheres 
agraphia.       III,      228;     XXI,      1304; 

xxn,  1377 

alexia.    III,    229;     XIII,    ^^T,   XXH, 

1403 
angular  gyrus,  XXII,  1493 
aphasia,   motor.   III,   222;    XIII,   774; 

XXI,  1304;  XXII,  1402 
sensory,  III,  223;  XIII,  775-6;  XXI, 

1306;   XXII,   1358-82 
arm   center,   XXII,    1362-6-83-8-91-3-9, 

141 1 
astereognosis.     III,     230;     VI,     354; 

XXII,  1359-83 

blindness,    psychic.     III,     232;      XXI, 

1307;    XXII.    1357-81 
calcarine    fissure,    XXII,    1378-9-80 
central     convolution,     anterior,     XII, 
1 385-8-91 -2-3-9,   1410-I- 

posterior,   XXII,    1361-2-5-83 
claustrum,  XXI,  1301 
corpus  callosum,  XXI,  1300 

striatum,   XXI,   1299;   XXII,   1398 
cortical    lesions,   XXI,    1308 
external  capsule,   XXI,   1301 
face   center,   XXII,   1392-9 
facial  fibers,  XXII,   1545 
frontal    convolution,    inferior,    XXII, 
1402 
middle,  XXII,  1401-9 
frontal    lobe,    XIV,   886;    XXI,    1304; 

XXII,  i40t-2 
geniculate  bodies,  XXII,  1337 

ganglion,   XXII,    I349-50 
hemianopia,   homonymous,   XIV,  817 ; 
XXI,  1298,  1307,  1337;  XXII,  I35S- 
6: 
See   also  hemianopia 


283 


INDEX 


Localization,  internal  capsule,  XIV,  86l ;  XXI, 
IZ99;   XXII,   1367-74-97 
island  of  Reil,  XXI  1301 
leg   center,   XXII,   1361-5-8-75-85-91-9, 

1412 
nucleus  caudatus,  XXI,  1299, 

lenticularis,   XXI,    1299 
occipital   lobe,    XIV,   850-3-6-7;   XXI, 

1307;  XXII,   1378-9-80-1 
optic   fasciculus   of    Gratiolet,     XIV, 
850-9-60;  XXII,  1378 
thalamus,  XXI,   1298,  XXII,   1398 
parietal    lobe,    XII,   657;    XXI,    1395; 
XXII.    1368;    1413-5 
lobule,   inferior,   XXII,    1375 
superior,    XXII,    1368 
pineal  gland,  XXI,  1303 
pituitary  gland,  XXI,  1302 
Reil,  island  of,  XXI,  1301 
temporal  convolution  or  lobe  superior, 
XIV,      923-243.-2$;     XXI,     1306; 
XXII.    1358-82 
cranium,  at  base  oi,  XXI,   1297 
Failure  of,  VI,  376 

Motor  paralysis,  XXII,   1315-16-17-19-20 
Neurons,  central,  XXII,   1313 
peripheral   XXII,   13:2 

brachial    plexus,    XXII,    1326 
Cauda  equina,   XXII,   1328 
chorda   tympani,   XXII,    1351-2 
cranial   motor  nerves,   XXII,    1323 

sensory  nerves,   XXII,   1321 
facial  nerve,  XXII,   1333-48  to  52 
hemianopia,    XXII     1331 :      See    also 

Hemianopia 
lumbar  plexus,  XXII,   1326 
optic       chiasm,       XIV,       854-64-5-94; 

XXII,    1335-6 
nerve,   XIV,  847-54-66;   XXII,    1334 
tract,  XIV,  862-2-3-95;   XXII,   1337 
orbit,  XIV,  915;  XXII,  1332-8 
ponto-cerebellar  angle  XVII,  1377 
sixth  cranial  nerve,  XXII,  1343 
spinal    nerves,    X,    489;     XIV,    824; 

XXII,   1323  to  8 
third  cranial  nerve,  XXII,  1339 
sensory     paralysis,     XXII,     1314-16-17- 

18-20 
Spinal  cord,  XX,  1250  to  79 
anterior       commissure,       XX,      1275 ; 
XXII,    1370-2 
horn,  XX,   1268;   XXII,   1324 
nerve  roots,  XXII,  XXII,  1324 
Burdach's   column,    XXII,    1322 
central  gray  matter,  XXII,  1370-2 
cervical       enlargement      and      region, 

XXII,    1330-63-4-71-2-86-9,    1407 
direct     cerebellar     tract,     XII,     653 ; 

1272 
dorsal   region,  XXII,   1360-9-84,   1404      I 


Localization,    lateral    column,    XXII,   1369-71- 
3-84-6-9,  1406 

li'mbar  enlargement,  XXII,   1329-70 
posterior  column,  XII,  654;  XIII,  786; 
XX,  1271;  XXII,  1322-60-3-4,1406 
horn,  XX,   1269;  XXII,   1322 
nerve     roots,     XX,    1298-9;    XXII, 
1322 
Segments 
cervical ; 
8th,   XX,    1263 
7th,  XX.   1264 
6th,  XX,  1265 
5th,  XX,   1266 
4th  to   1st,  XX,   1267 
dorsal ; 
I2th  to  3d,  XX,  1260 
2d,  XX,  1261 
1st,  XX,  1262 
lumbar; 
5th,  XX,  1250 
4th,   XX,   1251 
3d,  XX,   1252 
2d,  XX,  1253 
1st,  XX,  1254 
vision,  Dusturbances  of,  XIV,  808;  XXII, 

1331 
Localized  atrophies  and  hypertrophies,   XVII, 

1188 
Lockjaw:     See  tetanus 
Locomotor  ataxia  :     See  tabes 
Long  thoracic  nerve.  Paralysis  of,  XII,  709 
Lower  motor  neurons,  p.  9;  IX,  462 

sensory  neurons,  IX,  464 
Lumbar  enlargement :     See  spinal  cord 
plexus,  spasm  or  cramp  of,  XII,  733 

symptoms  of  lesions  of,  XXII,  1326 
puncture,  I,  74;  XI,  590 
Technic  of,  I,  74 
Results  of,  XIX,  1220 
Lumbo-abdominal   neuralgia,   XV,   990 
Lyssa,  II,  173;  XI,  604 

Macrocephaly,   I,  22 

Macropsia,  VI,  387 

Major  attack  of  epilepsy,  XI,  575;  XVI,  1061 

Mania,  p.  29;  III,  236 

Acute  alcoholic,   XVI,  1 109-12 

Epileptic,  XI,  575;   XVI,   1061-85,   1 104 

Primary.  XVI,   11 18 

Symptomatic,  or  delusional  or  secondary, 
XVI,   1 1 14 
Maniacal   excitation,   XVI,    11 18 

frenzy,   XVI,    1 1 18 
Manic-depressive   insanity,   XVI,    1120 
Marie-Tooth-Charcot's      type      of       muscular 

atrophy,  X,  496;   XII,  696 
Marie's    hereditary    cerebellar  ataxia,  II,   104- 
24;  XII,  650,  69;  XIII,  783 

ideas  of  aphasia,  XIII,  739 

reflex  of  spinal  automatism,  V,  328 


284 


INDEX 


Mask-like  face,  XI,  6io;  XII,  677;  XIII,  769, 

804 
Mastodynia,  V,  983 
Masturbation  in  nervous  diseases,  I,  2 
Mattoids,   XVI,   1095 
Maxillary   reflex,   V,   323 
Mechanical  irritability  of  nerves  and  muscles, 

I,  67 
Median  paralysis,  XII,  714 
Medulla  oblongata,   Hemorrhage  or  softening 
in,   X,   540-1-4;    XII,   749 
localizing  symptoms  :     See  localization 
Tumor  of,  X,  541;  XII,  656;  XIII,  749 
Meig's  disease,  XVII,  1202 
Melancholia,  p.  29;  III,  234 
agitata,   XVI,   11 15 
attonita,  XVI.  1115 
cum  stupore,   XVI,   1115 
Primary,  XVI,  11 17 
raptus,  XVI,  11 15 

Secondary,    or    sympathetic,    or     sympto- 
matic, or  delusional,  XVI,   1 1 15 
Memor>',p.  17 

Disturbances  of,  I,  i ;  III,  203 
Tests  of,  I,  6 
Mendel-Bechterew's    reflex :     See    dorsal    foot 

reflex 
Meniere's    disease,    XII,    649-85;    XIV,    918; 

XV,  1019 
Meningeal    apoplexy,    II,    147-89;    X,  502-24; 

XI,  588 ;  XIV,  1063 
Meningismus,  XI,  594 

Meningitis,   II,   119-23-48-67-76-86-92;   X,  508; 
XI,  590-1,  605;  XVI,  1045 
Cerebral,  X,  508;  XI,  590,  605;  XFV,  834; 
XV,  1033;  XVI,  1045;  XVIII,  i2o8-9r 
14-^6  to  29 
Vertigo  in,  XV,  1033 
Cerebro-spinal,     XI,     591,     605;     XVIII, 
1214;  XIX.  1226  to  29 
fluid  in,  VIII,  405-9-10-1-2;   XIX,   1226 
to  29,   1332 
gummosa,  II,   176;   XVIII,   1208-9-13-14 
Headache  in,  XV,  963-6 
Localized,  X,  508 
Optic  neuritis  in.  XIV,  906 
Purulent,  II,  192;  XI,  592;  XIX,  1227 

Cerebro-spinal  fluid  in,  XIX,  1241 
Spinal,  acute  and  chronic,  XI,  605 ;  XV, 

974,    1 105;   XVIII,    1213-4 
of   spinal    cord    and    nerve    roots,  XVIII, 

1213 
Syphilitic,  XV,  981 ;  XVIII,  1208-9-13-14 
Tuberculous,  II,  119-23-92;  XI,  593;  XIX, 
1228-9 
Cerebro-spinal  fluid  in,  XIX,   1228-9 
Meningocele,  II,  102 

Mental    activity,    Disturbances    of,    I,    I ;    III, 
200;  XVI,  1036 
Diseases  causing  disorders  of,  XVI,  1036 
Reaction  time.  Tests  for,  i,  s 


Mentality,  Weakened,  XVI,  1040 
Meralgia  paresthetica,   XV,  999 
Mercurial  tremor,  II,  160;  XII,  673 
Metamorphopsia,  VI,  385 
Metastasis  in  nervous  diseases,  II,  98 
Metatarsalgia,   XV.   1003 
Microcephaly,  I,  22;   XVI,   1084 
Micropsia,  VI,  386 
Microsmia,  XVII,  1177 
Migraine,  II,  1 15 ;  XV,  950,  1029 
Glittering  scotomata  in,  XIV,  849 

Hemianopia  in,  XIV,  858 

Vertigo  from.  XV.  1029 

Millard-Gubler's  s>'ndrome,  IX,  429;  XXI, 
1229 
Milroy's  disease,  XVII,  1202 
Miner's  nystagmus,  XII,  684 
Minor  attack  of  epilepsy,  XI,  575 ;  XVI,  1061- 

73 
Miosis,  I,  24;  V,  340;  XII,  661;  XVII,  1191; 

XXI,    1290 
Mixed  aphasia.  III,  225;  XIII,  778 
Mobile  spasm,   IV,  271 
Mongolism,   XVI,   1095 
Monocular  diplopia,  VI,  381 ;  XIV,  818 
Monoplegia,  IV,  258;  X,  478-9-81,  527;  XIII, 
796 
Diseases  causing,  X,  47S-9-81 
Hysterical,   X,  527;   XIII,  796 
Organic,  XIII,  797 
Moral  imbecility  and  insanity,  p.  28;  XVI,  1096 

sense,  Tests  for,  I,  5 
Morons.  XVI,  1095 
Morphine  headache,  XV,  954 

vertigo,  XV,   1 03 1 
Morton's  toe,  XV,  1003 
Morvan's    disease :     See    Sj'ringomyelia, 
Motion,    Diseases  causing  diminution  of,  IV, 
244;  X,  469;  XXII,  1315-6-9-20 
Exaggeration    of,    IV,    245-7;    XI,     570; 

XXII,  1311 
Perversion  of,  IV,  243;  XII,  635 
Disorders  of  voluntarv-,  IV,  240;  X,  469; 

XI.  570 ;  XII,  635;  Xni,  735 
Involuntary',  p.  35 
Motives,  Play  of,  p.  33 
Motor  aphasia,  III,  222;   XIII,  774 

Localization  of,  XXI,  1304;  XXII,  1402 
Ataxia,  IV,  280;  X,  488;  XII,  644;  XXI. 
1290  to  97 
Diseases  causing,  XII,  644 
Impulses,  Conduction  of,  p.  9 
Neurons,  p.  8,  9 
Diseases  of  the,  X.  469:  XI,  570;  XII, 
635-7 
-oculi.  Paralysis  of,  XII,  700 
paralysis,  IV,  244 :  X.  469 
Diseases  causing,  X,  469;  XXII,  1315-6- 

9-20 
Localization   of,   XXII,    1310 
Tests  for,  I,  34-5 


285 


INDEX 


paresis,  IV,  244;  X,  469 

points,  electrical,  I,  70-1 ;  VII,  393 
Movements,  p.  10 

Association,  p.  22 

Autochthonous,  p.  35 

Automatic,  p.  14,  35 

Involuntary,  p.  35 

Reflex  :     See  reflex 

Voluntary,  p.  14,  31 
Mowing  gait,  XIII,  797 
Mucous  membrane  reflex  acts,  V,  298 

Tests  for,  I,  58 
Multiple    encephalitis.    Acute,    X,    495,  543-4; 

XVI,  1046-7-8 
Myelitis :     See  sclerosis 
Neuritis :   See    neuritis 
Sclerosis :  See  sclerosis 

Muscae  volitantes,  XIV,  848 
Muscle  degeneration,  IV,  252;  XVII,  1131 
-joint  sensation,  p.  9 
sense,  Loss  of,  XI,  352;  X,  488;  XII,  661; 
XIV,  813 
Diseases  causing,   XIV,  813 
Tests  for,  I,  43 
tone,  I,  40;  IV,  240 
Muscles  and  nerves,   Electrical   reaction  of,  I, 
72 :  VII,  393 
Mechanical  excitability  of,  I,  67 
trophic    lesions    of,    Diseases  causing,    X, 
476-7;   XVII,   1 123 
Muscular  atrophy,  I,  41 

Aran-Duchenne's    type    of,    X,    548;  XII, 

694-5;   XIII,  800,  XVII,   iiso-i 
Charcot  Marie-Tooth's    type    of,    X,    496; 

XII,  696 

in  chronic  paralysis,  XVII,   1155 

Dise-ases  causing,  X,  476-7;   XVII,   1131 

from   disease,   XVII,    1155 

Idiopathic.  X,  498 

Landouzy-Dejerine  type  of,  X,  497;  XVII, 

"54 
Peroneal  type  of,  X,  496 ;  XII,  696        "~ 
Progressive,    spinal,    X,    547-8;  XII,  695; 

XIII.  800;   XVII.   1 150 

Spinal  or  neuritic,  X,  496;  XII,  696 
Muscular  coordination,   I,   47 

dystrophies,  II.  107-28;  X,  477;  XIII,  787; 

XVII,  1 154-8 
dystrophy,  Erbe's  juvenile  form,  or  scapu- 
lo-humeral    type,    X,  499;   XIII,  787; 

XVII.  1 154 

in  disease,  X,  477 

Landou7y-Dejerine's     form,     or     facio- 

scapulo-humeral   type,    X,    497;    XIII, 

787;   XVII,   1 154 
Pseudo-hypertrophic     form,     I,     21 ;     X, 

500;  XIII,  787;   XVII,   1 158 
Simple    or    idiopathic,    X,    498;     XIII, 

787;  XVII,   1 1 54 


Muscular  hypertrophy,   I,  40 

in  athletes,  XVII,   11 56 

Diseases  causing,  XVII,  1132 
Muscular  insufficiency,  ocular,  I,  24;  XII,  692; 
XIV,  818 

rigidity,  I,  31 :     See  also  paralysis  agitans 

tonicity.  I,  39;  IV,  240;  X,  472-3 
Musculo-cutaneous  paralysis,   XII,   713 

-spiral   paralysis,   XII,   716 
Mutism,  Deaf,  IV,  283 ;  XIII,  744 

Hysterical,  IV,  283;  XIII,  747;  XVI,  1076 

Insane,    IV,    283;   XIII,  746;   XVI,   1097, 
1104-5-15-17 
Myasthenia  gravis,  X,  554;  XIII,  764 

Tests   for,  I,  36 
Myasthenic  electrical   reaction,  VII,   399 

paralysis,  IV,  253;   X,  554;  XIII,  764 
Myatonia  congenita,  II,  105 ;  X,  483 
Mydriasis,  I,  24;  V,  339 
Myelitis  or  Myelomalacia,  II,  122-49-68-87 

in  anterior  horns :     See  poliomyelitis 

cervical     enlargement,     X,   550;    XIV, 
838;  XVII,  1149;  XXII,  1330 
region,   X,   413-4 

Compression,  II,  122;  X,  520;  XIII,  79$ 

Disseminated :     See  sclerosis 

in  dorsal  region,  X,  517-8;  XIV,  831 

above   lumbar   enlargement,   X,   513-14-17- 
18-20-50;  XIII,  708;  XIV,  830-1-8 

in    limibar    enlargement,     X,    485;     XIII, 
793;  XIV,  827;  XVII,  1 149;  XX,  1339 

Multiple:     See  sclerosis 

Transverse,  XV,  980 
Myoclonia,  XII,  697 
Myoclonic   nystagmus,   XII,   691 
Myoclonus,  IV,  270;  XI,  600-1 

epilcpticiis,  XI,  601 
Myokimia,   IV,  294;   XII,   697 
Myopia  and  cycloplegia,  V,  331 
Myotonia,  IV,  265 

acquisita,  XI,  611 

atrophica,  XI,  611 

congenita,    II,    106;    IV,    265;    XI,     6ri ; 
XVII,  1 1 57 

intermittens,   XI,  6tl 
Myotonic  electrical   reaction,  VII,  400 
Mysophobia,  III,  235;  XVI,  1074 
Myxedema,  I,  20;  XVII,   T163 

Nageotte  and  Babinski's  bulbar  syndrome,  IX, 

427:  XXI,  1290 
Nanosmia,  XVII,  ii77 
Narcotism,  II,  165;  XI,  585;  XV,  954;  XVI, 

1057 
Nasal    hemianopia,    VI,    362;    XIV,      817-65; 
XXII,   1336 
reflex,  V,  313 
Tests  for,  I,  58 
Neck,  Paralysis  of  muscles  of,  XII,  705 
Spasm  of  Muscles  of,  XII,  730 


286 


INDEX 


Negativismus,   XVI,   1098  to  iioi 
Nerves  and  muscles,  Electrical  reaction  of,  I, 
71-2;   VII,  393 
Injury    of,    X,  489-92;   XIV,  824;   XVII, 
1 146-7;    XXII,    1323-7 
Nerves  and  muscles,   Symptoms  of  lesions  of 
nerves, 
Motor  cranial,  X,  452 ;  XXII,  1323-7 
Facial,  XII,  703;  XIII,  754;  XIV,  928; 

XXII,   1333-48  to  52 
Sixth     (abducens),    XIV,    872;    XXII, 

1343 

Third.  XII,  700;  XIV,  873  to  yT,  XXII, 
1339-42 
Root,  anterior,  XX,  1279 ;  XXII,  1324 

posterior,   XIV,  826;   XX,   1278;   XXII, 
1322 
sensory,  cranial,  XXII,  1322 
spinal,   X,   489;   XIIc   and   d;   XIV,  824; 

XXII,      1323-5-7 :  See     also    neuralgia, 

neuritis  and  tabes 
Nervous  system,   Physiology  of,  p.  5 
Neuralgia,  I,  2;  II,  1 15-71;  XV,  933-37 
Achillodynia,  XV,  1001 
Angina  pectoris,  XV,  984 
Arthralgia,  XV,  looo 
Calcanodynia.    XV,    1002 
Causalgia,   XV,   1003a 
Coccygodynia,  XV,  972 
Cervico-brachial,    XV,    995 
Crural,   XV,  997 
Enteralgia,   XV,  989 
Erythromelalgia,  XV,  loio;  XVII,  1 198 
Gastralgia,    XV,   987 
Genital,  XV,  991 
Herpetic,  XV,  940-78 
Hysterical.   XV,  951-71,    1000 
Idiopathic,    XV,   937 
Infra-maxillary.    XV.    946 
Infra-orbital,  XV,  945 
Intercostal,  XV,  977 
Intestinal,  XV,  989 
Joint,  XV,   1000 
Lumbo  abdominal,    XV,   990 
Mastodynia.  XV.  983 
Meralgia  paresthetica,  XV,  999 
Metatarsalgia,  XV,  1003 
Neurasthenic,    XV,   960-70 
Obturator,   XV,  998 
Occipital,  XV,  949-53 
Pelvic,  XV,  953-91 
Phrenic,  XV,  986 
P.seudo -angina  pectoris,  XV.  985 
Sciatica,  XII,  720;   XV,  996 
Spinal,   XV,  971 
Supra- orbital,   XV,  944 
Symptfmatic,  XV,  937-53 
Syphilitic,  XV,  952 
Tabetic,   XV,  979-88,   T004 
Talalgia,  XV,  1002 
Thermalgia,  XV,   1003a 


Neuralgia,  Tic  douloureux,  IV,  267;  XI,  599; 
XII,  726;  XV,  948 

Trigeminal,  XV,  943  to  47 
Neurasthenia,   II,    114-56-62-64-81-3 ;   XV,  560- 
70;    XVI,   1074 

Perversion  of  vision  in,  XIV,  846-8 
Neurasthenic  backache,  XV.  970 

headache,  XV,  960 

tremor,  XII,  671-4 

vertigo,  XV,  1034 

Neuritic  electrical  reaction,  VII,  401 

or  spinal  muscular  atrophy,  X,  496;   XII, 
696 

Neuritis,   II,   141-3-5-51-66-77-88;   X,  488-9-92; 

XIV,  824;  XV,  933-41-9,  XVII,  1147-73; 

XXII,  1321  to  27 
Alcoholic:     See  multiple  neuritis 
Anterior  crural,  XV,  997 
Arsenical,  II,  158:     See  multiple  neuritis 
Brachial  plexus,  X,  490 
Causalgia,  XV,  1003a 
Compression,  XV,  939 
Crural.  XV,  997 

Diabetic.      II,      194:  See     also      multiple 

neuritis 
Diphtheritic,     X,    488;     XIII,   756-7:  See 

also  multiple  neuritis 

Erythromelalgia,  XV,  loio;  XVII,  1198 

Herpetic  ganglionitis  or  neuritis,  II,  141-3- 

5-51-8-66-88-94;     XV,    5WO-78,    XVII, 
1 166 

Cerebro-spinal  fluid  in,  XIX,  1235 
Infra-maxillary,   XV,  946 

-orbital.  XV,  945 
Leprous,  II.  141;  XVII,  1169 
Multiple,    II,    140- 1 -58-61 -77-94;     X,    488; 

XII,  662;  XIII,  756-7-89;  XIV,  82s,  XV, 

952-1008;    XVII,    1 147;    XVIII,    I2is; 

XXII,  1327 
Occipital,  XV,  049 
Optic,  X,  S07-8;  XIV,  892.  910 

tract,  XIV,  862-3-95;  XXII,   1337 
Simple     XV,     933-41-9;    XVII,     1 147-73; 

XXII.  1321  to  27 
Supra-orbital,  XV,  944-53 
Syphilitic,   II,   177;   XVIII,   1215 
Trigeminal.  XV,  943  to  48 
Neuroma.  X,  491  ;  XV,  938 
Neurons,  p.  6 

Centrifugal,  p.  9 
Centripetal,  p.  6 
Diseases  of  the, 

central,  X,  473-4;   XXII,  1313 

motor,    p.    8,    9;    IV,    251-2;    IX,  461-a 
X,  460-72-3;   XVII,   1 131 

peripheral.  X,  472-4;   XIV,  805;   XXII, 
1312 

sensory.  VI.  344:   IX.  463-4;   XIV,  805 
Neuroses,  II,  133-8 

Occupation.  II,   144:   XI.  615 

Traumatic.  II.   157;  XII,  674;  XV,  1034; 

XVI,  1074-7 


287 


INDEX 


Neurotonic  electrical  reaction,  VII,  401 
Nicotine  tremor,  XII,  673 

vertigo,   XV,   1031 
Nictitation,   XII,  726 
Nictitatio  spastica,  XII,  679-90,  726 
Nocturnal  epilepsy,  XI,  575 ;  XVI,  1061 
Nonne-Apfelt  test,  VIII,  412 
Nuclei,  Symptoms  of  lesions  of 

cranial,  X,  493;  XXII,  1321-2-4 
motor,  X,  493;  XXII,  1324 
Facial,  XXII,  1347 
Sixth,  XXII,  1343 
Third,  XXII,  1339-42 
sensory,  XII,  1322 
Spinal 

motor,  XXII,  1324-7 :     See  poliomyelitis 
sensory,  XXII,  1322-7 :     See  tabes 
Nucleus  caudatus  and  lenticularis :     See  locali- 
zation 
Numbness,  VI,  375;  XIV,  814 
Nyctalopia,  VI,  361 

Nystagmus,  I,  24,  31;  IV,  292;  XXI,  1294-5 
Cerebellar,  I,  80 
Diseases  causing,  XII,  640 
Miner's,  XII,  684 
Myoclonic,   XII,  691 
Tests  for,  I,  24,  31,  80 

Observation,   Delusion   of,   XVI,    1 1 16 

Tests  for  power  of,  I,  s 
Obstetrical  hand,  XI,  612 

paralysis,  IX,  444-5 ;   X,  490 
Obturator  neuralgia,  XV,  998 

paralysis,   XII,  718 
Occipital  headache,  XV,  949-53 

lobe,  SjTnptoms  of  lesions  of,  XIV,  850-3- 
6-7;  XXI,  1307;  XXII,  1378-9-80-1 

neuralgia  or  neuritis,  XV,  949-53 
Occupation  in  nervous  diseases,  I,  2;  II,  90 

neuroses,  II,  144;  XI,  611 
Ocular  ataxia,  XII,  648 

headache,   XV,  953 

muscles.  Insufficiency  of,  XII,  692;  XIV, 
818 
Paralysis  of,   XII,  700;   XIV,  818-72-7; 

XXII,   1332 
Spasm  of,  XI,  590;  XIV,  818-78 

vertigo,  XII,  648;  XV,  1020 
Oesphageal  spasm,  XI,  616 
Olfaction,  Cortical  center,  p.  8 
Olfactory  sensation,  p.   8 
Ontogenetic  acts,  p.   II 
Ophthalmoplegia    completa,    X,    545 

externa,  X,  545;  XI,  590;  XIV,  872 

interna,  X,  545;  XI,  590;  XIV,  873 

progressiva,  X,  545 

sympathetica,  XXI,  1290 
Ophthalmoscopic    examination.     Diseases     re- 
vealed by,  I,  76;  XIV,  821 
Opisthotonos,   IV,  265 ;   XI,  590,  603-13 


Opium  poisoning,  XVI,  1057 
headache  from,  XV,  954 
tremor  from,  XII,  673 
Oppenheim's  disease,  X,  483 

reflex,  I,  57;  V,  306 
Optic  aphasia.   III,  224;   XIII,  776 
atrophy,  XIV,  893,  911 
chiasm,  p.   8 

symptoms  of  lesions  of  the,   XIV,  854- 
64-S;  XXII,  1335-6 
fasciculus    of    Gratiolet,    Lesions   of  the, 

XIV,  850-960;  XXII,  1378 
nerve.    Lesions    of    the,    XIV,  847-54-66; 

XXII,  1334 
neuritis.  Diseases  causing,  X,  507-8;  XIV, 
892 
atrophy  following,  XIV,  910 
papilla,  Abnormalities  of,  XIV,  821 
thalamus.    Symptoms   of   lesions   of,    XII, 
655;  XXI,  1298;  XXII,  1398 
Localization  in  :     See  localization 
tract,  p.  8 

Symptoms  of  lesions  of,  XIV,  862-3-95; 
XXII,   1337 
Orbit,  Symptoms  of  lesions  within,  XIV,  915 ; 

XXIL  1338 
Organic  diseases,  II,  137-9 
hemiplegia,  XIII,  797 
reflex  acts,  I,  i ;  V,  300-24-5 ;  X,  476 ;  XIV, 
Sii 
Orthotonos,  IV,  265 ;  XI,  590,  603-13 
Oscedo,  XII,  731 
Osseous  sense.  Loss  of,  VI,  353 

Tests  for,  I,  56 
Osteitis  deformans,  XVII,   1182 
Osteo-arthropathy,     Hypertrophic     pulmonary, 

XVII,  1 184 
Osteogenesis    imperfecta,    XVII,    1185 
Osteomalacia,  XVII,  1185 
Osteopsathyrosis,  XVII,   1 185 
Ovarian   tenderness,    IX,   415 
Oxyakoia,  XIV,  823 

Pachymeningitis,  X,  502 ;  XI,  588 ;  XVI,  1063 
Headache  in,  XV,  963 
hypertrophica  cervicalis,  X,  551 
interna    hemorrhagica,    X,    502;   XI,  588; 
XVI,  1063 
Paget's  disease,  XVII,   1182 
Pain,  p.  7;  I,  I,  50;  VL  374-80 
Diseases  causing,  XV,  931 
in  abdomen,   XV,  935 
back,  XV,  935 
extremities,  XV,  936 
head,  XV,  934 
nerve  distribution,  XV,  933 
thorax  and  abdomen,  XV,  935 
trunk,  XV,  935 
Girdle,  VL  374;  XV,  976  to  82 
Persistence  of,  I,  52;  VI,  382 


288 


INDEX 


Pain,  Radiating,  VI,  374 

Referred,  VI,  374;   XV,  953 
Retardation  of  conduction  of,   I,  51 ;   VI, 
381 
Palatine  arch,  High,  XVI,  1078 
Pallesthesia,  Loss  of,  V,  353 

Tests  for,  I,  56 
Palpation  in  examination,  Ic 
Palsies,    Local,    IV,    259;    X,  481;  XI,  571-2; 

XII,  636 
Pantophobia,   III,  235 
Papilla :     See  Optic     papilla 
Paradoxical  pupillary  reflex,  V,  338 
reflex,   V,  318-9-38 
sensation,    VI,    379 
Parageusia,  VI,  391 
Paragraphia,  III,  227;  XIII,  780 
Parakinesis,  IV,  243 
Parakusis,  VI,  389;   XIV,  823 

Diseases   causing,   XIV,  823 
Paralysis,  I,  1-21 ;  IV,  244 

Abducens,  XII,  701 ;  XIV,  872 
Abductor  laryngeal,  XIII,  759 
Acute  ascending,  II,  170;  X,  482 
Agitans,  I,  20-1;  XI,  610;  XII,  677;  XIII, 

769,  804 
Alcoholic :     See  multiple  neuritis 
Arsenical :     See  multiple  neuritis 
Atonic,  IV,  252;  X,  472 
Atrophic,  IV,  252;  X,  472-6-7,  547-8 
Acute:     See  poliomyelitis 
Chronic :     See     chronic     atrophic     and 
bulbar   paralysis 
Axillary,  XII,  712 
Bell's,  XII,  703 
Brachial  plexus,  IX,  414-5;  X,  490;  XXII, 

1326 
Brown-Sequard's,   IX,  432;   X,  509;   XIV, 

844;  XV,  982 
Bulbar,  IX,  424;  X,  544-6;  XH,  694;  XIII, 

759-64;    XVII,    1 151 
Cauda    equina,    X,    487;    XII,    721;    XV, 

1007;  XXn,  1328 
Cervical  rib,  X,  557 

sympathetic,   IX,   455;   XVII,   1191 
Choreic,  X,  510 
Chronic 

bone  atrophy  in,  XVII,  1139 
Muscular  atrophy  in,  XVII,   1155 
continuous,   Diseases   causing,   X,  470 
Crico-ar>-tenoid,  XIII,  759 

-thyroid,   XIII,  757 
Crossed,  IV,  256;  X,  535  to  41 ;  XV,  1017; 

XXI,  1290  to  93 
Crural,  XII,  717;  XV,  997 
Diaphragmatic,  XII,  707 
Diphtheritic,  XIII,  756-7:     See  also  mul- 
tiple neuritis 
Diseases  causing,  IV,  244;  X,  469;  XIV, 

805;  XXII,  1310 
Diver's,  X,  521 


iParalysis,  Erb's,  IX,  444;  X,  490 

I        External   rectus,   XII,  701;   XIV,  782 

Facia'.,    XII,    703;    XIII,    754;  XIV.  928; 

XXII,  1333-45  to  52 
Family  periodic,  X,  556 
Flaccid,  IX,  252 

Diseases  causing,  X,  472 

Test?  for,  I,  34  to  41 
Foville's,  IX,  454;  XXI,   1292 
Glosso-pharyngeus,  XII,  703a 
Gluteal,  XII,  719 
Hand,  XII,  714-16 
Hj-pertonic,  IV,  251 ;  X,  473 
Hypoglossal,  XII,  706;  XIII,  755 
?lypotonic,  IV,  252;  X,  472 
Hysterical,  I,  21;  IX,  415;   X,  527;  XIII, 

747-S-62-96;  XIV,  880;  XVI,  1076 
Infantile :     See  poliomyelitis  and  cerebral 

palsy  of  childhood 
Inferior  oblique,  XIV,  877 

rectus,  XIV,  875 
Intermittent,  X,  471 
Internal  rectus,  XIV,  873 
Klumpke's,  IX,  445 ;   X,  490 
Labio-glosso-ipharyngeal-laryngeal,  IX, 

412;  X,  546;  XII,  694;  XIII,  759-64; 

XVII,  1151 
Landry's,  II,   170;  X,  482 
Laryngeal  nerve.  Recurrent,  XIII,  758 

Superior,  XIII,  757 
Lead,    II,    159;    X,    494;  XII,  716;  XIII, 

790;  XVI,  1053 
Levator   palati,    XIII,   756 
Local,   IV,  259;   X,  481;   XI,  571-2;   XII, 

700  to  721 
Localization  of  lesions  causing,  XXII,  1310 
Median,   XII,  714 
Motor,  IV,  244;  X,  469;  XXII,  1315-6-9- 

20 
Tests  for,  I,  34-5 
Motor-oculi,    XII,   700;   XIV,   873  to  JT, 

XXII,  1339  to  42 
Musculo-cutaneous,  XII,  713 

-spiral,   XII,   716 
Myasthenic,  IV,  253;  X,  554;  XIH,  764 
Neck  muscles,  XII,  705 
Obstetric,  IX,  444-5 ;  X,  490 
Obturator,    XII,    718 
Peroneal,   XII,  720 
Phrenic,  XII,  707 

Pneumogastric,   XII,   704;   XIII,   763 
Posticus  laryngeal,  XIII,    759 
Pseudo-bulbar,   X,   554;   XIII,   764 

-hypertrophic,     X,     500;     XIII,    787; 
XVn,    1 158 
Pterygoid,    XII,    702 
Radial,  XH,  716 
Rectus  externus,  XIV,  872 

inferior,   XIV,  875 
oblique,  XIV,  877 

intemus,   XIV,  873 


289 


INDEX 


Paralysis,  Rectus,  superior,  XIV,  874 
oblique,  XIV,  876 
Recurrens,  XIII,  758 
Sciatic,  XII,  720 
Sensory,  Diseases  causing,  VI,  345 ;  XIV, 

805,   XXII,    1314-6-8-20 
Serratus,  XII,  709 
Spastic,  IV.  251  ;  X,  473 
Spinal  accessory,  XII,  705 
Sub-scapular,   XII,   711 
Superior  larjngeal  nerve,  XIII,  757 

oblique,  XIV,  876 

rectus,  XIV,  874 
Supinator  longus,  XII,  716 
Supra-scapular,    XII,    708 
sympathetic     ganglia,     Diseases      causing, 

XVII,  1 142-91 
Tests  for,  I,  34-5 

Thoracic    (anterior    and    posterior),    XII, 
710 
Long,   XII,   709 

Thyreo-ary-epiglottis,   XIII,  757-602 

Tibialis,    XII,    720 

Trigeminus   (motor  branch),  XII,  702 

Trochlearis.  XV,  701 

Ulnar,  XII,  715 

Vagus,  XII,  704;  XIII,  763 

Vaso- motor,  V,  327 
Paralytic  dementia  :     See  paresis 

and  flaccid  gait,  XIII,  741 
spastic  gait,  XIII,  742 

vaso-motor    reflex,    V,    301-27 
Paramyoclonus  multiplex,  XI,  600-1 
Paramyotonia  congenita,  II,  106;  IV,  265;  XI, 

611 
Paranoia,  XVI,  11 16 
Paronoiacs,  p.   29 

Paranoid  form  of  insanity,  XVI,  iioi 
Paraphasia,  III,  226;  XIII,  778 
Paraplegia,  I,  21 ;  IV,  257;  X,  480 

Ataxic,  X,  526;  XII,  660;  XIII,  799 

Diseases  causing,   X,  474-80-1-2-84  to  88; 
XIII,  741-2;  XV,  975-80;  XXII,  1384-7 

dolorosa,   XV,  975 

Senile,  X,  522;  XIII,  794 

Spastic,  X,  525-47;  XIII,  800 
Paresis,  p.  29;  II,  135-80;  XI,  579;  XII,  675; 
XIII,  766;  XIV,  897;  XVI,  1052,  1106; 

XVIII,  1216;  XIX,  1230 
Cerebro-spinal    fluid    in,    VITI,   409-12-3-4; 

XIX,  1230 

Motor,  Diseases  causing,  IV,  244;  X,  469 
Tests    for,   I,   35 

Optic   atrophy  in,   XIV,  913 
Paresthesiae.  p.  7;   VI,  375 
Parietal  lobe  and  lobule :  See  localization 
Parkinson's  disease:     See  paralysis  agitans 
Parosmia,  VI,  390 
Passive  contracture.   I,  .38;   IV,  263 

Tremor,  IV,  290;  XII,  646,  646a 
Diseases  causing,  646,  646a 


Pelvic  neuralgia,   XV,  953-91 

Pemphigus,  XVII,  1 168 

Pendular  knee-jerk,  I,  61 

Perceptions,  p.  16 

Percussion  in  examination  of  nervous  diseases, 

Ic 
Perforating  ulcer,   XVII,   1172 
Periodic   family  paralysis,   X,  556 
Peripheral    neurons.    Disorders    of,  X,    472-4; 
XIV-80S 

Location  of  lesions  of,  XXII,  1312 

Motor  neurons,  IX,  462 
Diseases   of,   X,   472-4 

Sensory  neurons,  IX,  464 
Diseases  of,  XIV,  805 
Peroneal  paralysis,  XII,  720 
Peroneal    type   of   muscular   atrophy,   X,   496; 

XII,   696 
Persecution,    Delusion   of,    XVI,    1 1 16 
Persistence  of  sensation,  I,  52 ;  VI,  382 

Tests  for,   i,  52 
Personal  factors  in  nervous  diseases,  I,  2;  II, 

82 
Personality,    p    25 

Double,  III.  209;   XVI,  1039 

Diseases  causing.  XVI,   1039 

Erroneous,  III,  208 

Diseases  causing :     See  insanity 
Pes  calcaneus  et  valgus,  XII,  720 

equino-varus,   XII,  720 
Petit  mat   (le),  XI,  575;  XVI,  1061 
Pharyngeal   crises,   IX,  423 

reflex,  V,  316 
Pharynx,  Spasms  of  muscles  of,  XII,  727        ' 
Pharynx,   Paralysis  of,   XII.   703a 

spasm  of,  XII,  727 
Phobias,   III,  235;   XVI,   1074 
Photophobia,  VI,  371  :  XII,  683 
Phrenic  neuralgia,  XV,  986 

paralysis,  XII.  707 

spasm  or  cramp.   XII,  731 
Phylogenetic  acts.  p.   11 
Physical  exarrination  of  patient,  I 
Physiological    introduction,    p.   S 
Pianist's   cramp.   XI.  615 
Picric  acid  poisoning,  XIV,  845 
Pill-rolling  movement  of  fingers,  XII.  677 
Pineal  gland.  Diseases  of,  XXI.  T303 
Pituitary  gland.  Diseases  of  the,  XXI,  1302 

enlarged.  Symptoms  of,  XIV,  864 

Kunucbism   from  disease  of,  XVII,   1176; 
XXL    1302 
Plantar  reflex,  V,  303 

Tests  for,  I,  57 
Play  of  motives,  p.  33 
Pleasure,  p.  21 

Plcurosthotonos,  IV,  265 ;  XL  590.  603 
Plexuses.  Brachial  and  Lumbar,  Symptoms  of 

lesions  of,  IX,  444-51   X,  490;   XII,  733; 

XXII,  1326 


290 


INDEX 


Pneumogastric  paralysis,  XII,  704;   XIII,  763 

spasm   or  cramp.  XII,  728 
Points    of    Valleix,    XV,    937-43-49-7"-90-5-7 
Poisons,  I,  l;  II,  92,   165;  X,  482;  XII,  633; 

XIV,  845;  XVI,  1058 
Polioencephalitis   inferior.   Acute,   X,   534-44 
Chronic,    X,    546;    XII,    694;    XIII,  764; 

XVII,  nsi 
superior.  Acute,  X,  543 ;  XVI,  1046-8 :  See 
also  Botulismus  and  encephalitis 
chronic,  X,  545 
Poliomyelitis,    Acute    anterior,    II,    118-69;    X, 
1(^5;    XIII,    797;    XVII,    1148;   XIX, 

1^33 
Cerebro-spinal   fluid  in,   VIII,  409-12;   X, 

495;  XIX,   1233 
Chronic,  X,  548;   S48b 
Infantile   hereditary,    (family),    X,   548a 
Polyesthesia,  I,  54;  VI,  378 
Polyneuritis,     II,     140-1-58-61-77-94;     X,   488; 

XII,  662;  XIII,  756-7-89;  XIV,  82s;  XV, 
g;52-ioo8;  XVII,  1147-69;  XVIII,  1215; 
XXII,    1327 

Polyopia,  VI,  384 ;  XIV,  881 

Pons  Varolii,  Hemorrhage  or  softening  in,  X. 

538-9-43;   XIII,   749;   XIV,  843-85;   XXI. 
1292 

Localizing  symptoms  of:     See  localization 

Symptoms    of    lesions    of,    XIV,    843-85; 
XXII,   1344-46-66-76-95,   1401-8 

Tumor  in,  X.  539 ;  XII,  656 
Ponto-cerebellar  angle.  Symptoms  of  lesions  of, 

IX,  428;  XXII,  1377 
Ponto-spinal  tract,  the,  p.  10 
Porencephalic  idiocy,   XVI,   1088 
Porencephaly,  II,   117;  X,  501;   XI,  577,  631; 

XIII,  801 ;  XVI,  1088 
Position  sense.  Tests  for,  I,  41 
Post-epileptic  insanity,  XI,  575;  XVI,  1061 

coma,  XI,  575;  XVI,  io6i 
-febrile   insanity,    XXI,    1 1 10 
-hemiplegic  ataxia,  XII,  655 
athetosis,  XI,  631-2 
chorea,  X,  501  ;  XI,  626 
contracture,  X,  501-4;  XI,  577,  614-9 
-neuritic  contracture,  XI,  621 
-paraplegic  contracture,  X,  480,  516  to  20; 
549  to  52;  XI,  620;  XIII,  742 
Posterior  column  or  horn:     See  Spinal  cord 
inferior  cerebellar  artery,   Thrombosis  of, 

XXI,  1291 
longitudinal  bundle.  Lesion     of,  XIV,  885 
spinal  ganglion,  Lesion  of,  XX,   1277 
Postero-lateral    sclerosis,    X,    526;   XII,  660; 

XIII,  799 
Posticus    (laryngeal)    paralysis,   XIII,  759 
Pott's  disease,  I.  23 ;  II,  121 ;  X,  520 
Predilection   muscles    (Wernicke's).  IV,  254 
Predisposing    factors    in  nervous  diseases,  II, 

82 
Preputial   irritation,  IV,  251 


Pressure  sensation,  p,  6 
Pressure  sense.  Loss  of,  VI,  351 

Tests  for,  I,  49 
Priapism,  X,  512-5-49-52;  XI,  604;  XIV,  830 
Primary   dementia,    XVI,    1097 
Procursive  epilepsy,   XI,   575 
Prodromata  of  apoplexy,  IX,  422 

of  epilepsy,  IX,  420 
Progeria,  XVI,  1095 

Progressive  bulbar  paralysis,  IX,  424;  X,  546; 
XI],   694;    XllI,   759-64;    XVII,    1151 
lenticular  degeneration,  XII,  668 
muscular    atrophy,    X,    547-8;    XII,  695; 

XIII,  800;  XVII,   1150 
ophthalmoplegia :       See    polioencephalitis 
superior  chronica 
Propulsion,  XI,  610;  XII,  677;  XIII,  769,  804 
Prosopalgia,  XV,  943  to  48 
Prosopoplcgia,  XII,  703 
Protopathic  sensibility,  p.  7 
Pseudo-angina  pectoris,  XV,  985 

-bulbar  paralysis,  X,  546,  554;  XIII,  764 

-chorea,  XI,  573 

-clonus,  IX,  415 

-coma,  Diseases  causing,  XVI,  1038 

-hypertrophic     paralysis,    I,    21;    X,    500; 

XIII.  787;   XVn,   1158 
-nystagmus,  XII,  640 
-paresis,  XVI,  1103;  XVIU,  1208 
-ptosis,  XVII,  1191;  XXI,  1290 
-tabes :     See   multiple  neuritis 
Psychalgia,  XVI,   11 17 
Psychasthenia,  V,  970;   XVI,   1074 
Psychic  blindr.ess,  p.   17;  III,  232;  XXI,  1307; 
XXII,   1357 
deafness,    p.    17;    III,    223-33;  XIII,   775; 

XXI,   1306 
equivalent  of  epilepsy,  XI,  575 ;  XVI,  1061 
functions.  The,  p.  14 
trauma,   XVI,    1072-6 
Psychoanalysis,  I,  2 
Psychosis,  Korsakow's,  IX,  451;  X,  488;  XVI, 

1102 
Ptarmus,  XII,  728 
Pterygoid  paralysis,  XII,  700 
Ptosis,  I,  24;  XII,  700 
Puerperal   insanities,    XVI,    mo 
Pulmonary  osteo-arthropathy,   XVII,   1184 
Pupillary   abnormalities,    I,   24;    XIV,   820 
opening,    double.    XIV,  881 
reflex    acts 

Argyll-Robertson,    V,    332;    IX,    437; 

XIV,  891 
Accommodation,  I,  27;  V,  331 
Consensual,   I,  25 ;  V,  329 
Direct,  I,  25 ;  V,  329 
Hemiopic,  I,  26;  V,  334;  XIV,  890 
Indirect,   I,   25;   V,   329 
Light.  I,  25-7;  V,  329 
Pain,  V,  330 
Paradoxical,  V,  338 


291 


INDEX 


Pupillary  reflex  acts.  Pathology  of,  V,  302 

Physiology  of,  V,  302 

Westphal's,  V,  337 
Pupils,  Iirmobile,  V,  333;  X,  545 

Unequal,  V,  341 
Pulse  in  nervous  diseases,  I,  46 
Purulent  meningitis,  XI,  592;  XIX,  1227 

Cerebro-spinal   fluid   in,   XIX,   1227 
Pyramidal  tract,  Lesion  of,  XX,  1270 

Quadrantic  hemianopia,  VI,  363;  XIV,  816-56- 

7;  XXI,  1307;  XXII,  1356 
Quincke's  disease,  XVII,   1201 
Quinine  vertigo,  XV,   1031 
Quinquand's  sign,   IX,  443 

Rabies,  II,  173;  XI,  604 

Race  in  nervous  diseases,  II,  88 

Radial  paralysis,  XII,  716 

Radiculitis,  XV,  942 

Raptus  melancholicus,  XVI,   1115 

Raynaud's    disease,    XV,    loii;    XVI,     1059; 

XVII,   1 195 
Reaction    of    completely    degenerated    muicle, 
VII,  402 

of  degeneration.  Electrical,  VII,  397-8 
Reading,  Diseases  causing  disorders  oi,  XIII, 

735-77 
Tests  for,  I,  9 
Reasoning,  p.  33 
Receptors,   p.   11 
Recognition,  p.  17 
Rectal  crises,  IX,  423 

reflex,  V,  325 
Rectus  extemus  oculi.  Paralysis  of,  XIV,  872 
inferior,  XIV,  875 

obliquus.  XIV,  876 
internus,  XIV,  873 
superioris,  XIV,  874 
obliquus,  XIV,  876 
Recurrens  paralysis,  XII,  704;  XIII,  758 
Recurrent  insanity,  XVI,   1 1 20 
Red  nucleus.  Symptoms  of  lesions  of,  IX,  431 ; 
XXI,   1293;   XXII,   1341 
vision,  XIV,  846 
Referred  pains,  VI,   374 
Reflex 

Achilles,  I,  62;  V,  318 
Acts,  p.  14;  V,  296 

abolition     of.     Diseases     causing,     X, 

472;  XIV,  811;  XXII,   1312 
exaggeration.     Diseases     causing,    X, 

472;  XIV,  8ri;  XXII,  1313 
Inhibition  of,  V,  296-7 
Reinforcement  of,  I,  68 
Anal,  V,  307a 
Ankle,  I,  60;  V.  317-8 
arc,  p.   10;   V,  296 
Argyll-Robertson,    V,    332;    IX,    437; 

XIV,  891 
Association,  p.  14,  31 


Reflex,  Auditory-orbicularis,  V,  314 
Babinski's,  I,  57;  V,  304,  328 
Bechterew's,  I,  63 ;  V,  321 
Bladder,  V,  324 
Brissaud's,  V,  303 
Cilio  spinal,   V,   335 
Conjunctival,  I,  58;  V,  312 
Corneal,  I,  58;  V,  312 
Cortical,  p.  12 
Cremasteric,  I,  57;  V,  308 
Cutaneous,  I,  57;  V,  297 
Deep,  I,  60  to  68 ;  V,  299 
Defensive    (Babinski),    V,   327a 
Dorsal  foot,  I,  63 ;  V,  321 
Elbow,   I,  64;   V  322 
Epigastric,  I,  57;  V,  310 
Gluteal,  I,  57;  V,  307 
Gordon's,    V,   305 
Hemiopic,  I,  26;  V,  334;  XIV,  890 
Hyperemic,  V,  327;  XVII,  1130 
Inhibition   of,   p.    10 
Interscapular,  I,  57:  V,  311 
Ischemic,  V,  326;   XVII,    1 130 
Jaw,   I,  65;   V,  323 
Kemig's,  I,  66;  V,  320 
Knee,  I,  61 ;  V,  319 
Pendular,   I,   61 
Marie's,  of  spinal  automatism,  V,  328 
;  Maxillary,  I,  65 ;  V,  323 

Mendel-Bechterew's  I,  63;  V,  321 
Mucous  membrane,  I,  58;  V,  298 
Nasal,   I,  58;  V,  313 
Oppenheim's,   I,  57;   V,   306 
Organic,  I,  i ;  300-24-5 ;  X,  476 ;  XIV, 

811 
Paradoxical,  V,  318-9-38 
Pharyngeal,  I„  58;  V,  303 
Plantar,  I,  57;  V,  303 
J  Pupillary,  I,  25-7-8;  V,  302 

to    accommodation,    V,    331 
light,  V,  329 
Pain,  V,  330 
Rectal,  V,  325 
Reinforcement   of,    I,    68 
Spasm,  IV,  268;  XI,  616-8;  XII,  637; 

XVII,    1 194 
spinal  automatism    (Marie),  V,  328 
Sub-cortical,   p.    10 
Superficial,  I,  57;  V,  297 
Tendon,    I,    60-6;    V,    299;  X,  472-3; 

XIV,  811 
Umbilical,  I,  57;  V,  309 
Uvular,  I,  58;  V,  315 
Vaso- motor,  I,  59;  V,  301-27 
Vesical,   V,   324 
Westphal's  pupillary,  V,  337 
Wrist,  I,  64;  V,  322 
Reil,  Island  of.  Symptoms  of  lesions  of,  XXI, 

1301 
Reinforcement  of  reflexes,  I,  68 
Renal  crises,  IX,  423 


292 


INDEX 


Respiration,  Biot's,  IX,  425 

Cheyne- Stokes',  IX,  425;  XII.  728;  XXI, 
1290 

Tests  for,  I,  45 
Retardation  of  conduction  of  pain,  I,  51 ;  VI, 

381 
Retching,  V,  316 
Retina,    Perversion    of    vision    in  diseases  of, 

XIV,  847-83 
Retroactive  amnesia,  XIII,  772;  VI,  1102 
Retrograde  amnesia,  XIII,  772 
Retropulsion,  XI,  610;  XII,  677;  XIII;  769; 

804 
Reverie,  p.  24 

Rheumatism  of  scalp,  XV,  964 
Rhythmical  chorea,  XI,  629 
Rigidity,  I,  31;  IV,  266;  XI,  590,  603-S-10-12; 

XII,  677;  XIII,  769,  804 
Rigors,  XII,  680 
Rinne's  test.  I,  15 
Risus  sardonicus,  XI,  603 
Romberg's  symptoms,  I,  41 ;  IX,  438 
Rosenbach's  sign,  XVI,  1063-6 
Rotatory  epilepsy,   XI,   575 
Rubro-spinal  tract,   The,   p.   9 

Symptoms    of    lesions    of,    IX,  431 ;  XII, 
676;  XXI,  1293;  XXII,  1341 

Salaam  cramp,   XII,  690 

Saltatory  spasm,  XI,  618 

Sanity,  Tests  for,  I,  4 

Santonin  poisoning  or  jaundice,  XIV,  84S 

Scalp,  Localized  edema  of,  XVI,  1044 

Rheumatism    of,    XV,   964 
Scapulo-humeral    type    of    muscular   atrophy, 

X,  499;  XII,  787;  XVII,  1 154 
Schiiller's  side  gait,  IX,  456;  XIII,  796-7 
Sciatic  plexus.  Spasm  or  cramp  of,  XII,  733 
Sciatica,  XII,  720;  XV,  996 
Scissors  gait,  X,  501;  XIII,  798  to  803 
Schmidt's  syndrome,  IX,  450;  XII,  706 
Sclerodactyly,  XVII,  1165 
Scleroderma,  I,  20;   XVII,   1165 
Sclerosis,  Amyotrophic  lateral,  X,  547-8;  XII, 
695;  XIII,  800;  XVII,  1150 
Combined,  or  postero-lateral,  X,  526;  XII, 

660;   XIII,   799 
Disseminated,  or  multiple,  II,  150;  X,  511; 
XI,  580;  XII,  659-66-88;  XIII,  759- 
68,  803 ;  XIV,  914 ;  XV,  lois  ;  XVI, 
I0S4 
Optic  atrophy  in,  XIV,  914 
Vertigo  in,   XV,   1015 
Lateral,  X,  525-47 ;  XIII,  800 

Syphilitic  of  Erb,  X,  525;  XVIII,  1212 
Postero-lateral,    X,    526;    XII,   660,    XIII, 
799 
Scoliosis,  I,  23 
Scotomata,  Glittering,  XIV,  849 

Homonymous,    XIV,    867 
Scurvy,  X,  495 
Seamstress'  cramp,  XI,  615 


Secondary  dementia,  XVI,  1105 

deviation  of  sound  eye,  XIV,  818 
Tests  for,  I,  30 
Secretory   disorders,   Diseases   causing,   XVII, 

1 145 
Semeiological  charts.  Introduction  to,  p.  S 
Semi-coma,  III,  206 

Diseases  causing,   XVI,   615 
Senile  chorea,  XI,  625 

dementia,  p.  29;   XVI,   1107 
optic  atrophy,  XIV,  911 
paraplegia,   X,   522 
tremor,  XII,  678 
Senility,  Fragility  of  bones  in,  XVII,  1185 
Sensation,  p.  6,   15;  VI,  344;  XIV,  805;  XV, 
930 
Auditory,    p.    8;    I,    15;    HI,  223-33;  VI, 
355-72-89;    XIII,    744-75;    XrV,    809; 
XXII,  1382 
Conduction  of,  p.  7 
Cutaneous,  p.  6 
Deep,  p,  6 

Difficulties  in  testing,  I,  47 
Diminution  of,  I,  47;  VI,  345;  XIV,  806-II 
Diseases    causing,    XIV,  806;   XXII, 
1314-16-18-20 
Disorders  of,  VI,  344;  XIV,  805;  XV,  930 
Dissociation  of.  III,  209;  VI,  365 

Diseases    causing,    XIV,    812;    XXII, 
1354 
Double,  I,  54;  VI,  378 
Equilibrium,  p.  8 
Exaggeration  of,  VI,  346;   XIV,  807 

Diseases   causing,   XIV,  807 
General,  p.  9 
Gustatory,  p.  8;  I,  17;  VI,  357-70-9I ;  XV, 

810 
Hearing,  p.  8 
Internal,  p.   9 
Kinesthetic,  p,  7 

Light,  p.  10,  I,  12;  VI,  358  to  64-71-83  to 
87;  XIV,  808 
Disorders  of,   XIV,  808 
Localization  of,   I,  531   XXII,   1310-14-16- 

18-31 
Muscle-joint,  p.  7;  I,  43;  VI,  352;  X,  488; 

XII,  661 ;  XIV,  813 
Olfactory,  p.  8;  I,  16;  VI,  356-69-90;  XIV, 

810 
Painful,  p.  7 ;  VI,  374 ;  XV,  930 
Paradoxical,  VI,  379 
Persistence  of,  I,  52;  VI,  382 
Perversion  of,  VI,  347 

Diseases  causing,  XIV,  816;  XV,  930 
Pressure,  p.  6;  L  49)  VI,  351 
Sight,  p.  8 

Summation  of,  p.   II 
Tactile,  p.  6;  I,  48;  VI,  348-66-76  to  82 
Temperature,  p.  6;  I,  48-SS ;  VI,  350-68-79; 

XIV,  81 1 -2 
Visual,  p.  8 


293 


INDEX 


Sensibility,  Deep,  p.  6;  I,  43 

Epicritic,  p.  7 

Head's  researches  on,  p.  6 

Protopathic,  p.  7 
Sensory  aphasia,  p.  34;  I,  6;  III,  223-4;  XIII, 

775-6-7 

Locahzation  of,  XXI,  1306 ;  XXII,  1358-82 
Septic  insanity,  XVI,  mo 
Serous  niening^itis,  XI.  594;  XIX,  1241 

Cerebro-spinal  fluid  in,  XIX,  1241 
Serratus  paralysis.  XII,  709 
Sex  in  nervous  diseases,  II,  87 
Shaking  palsy :     See  paralysis  agitans 
Shell  shock,  XVI,  1077 
Shivering,  XII,  680 
Shock,  I,  I 

Shoemaker's   cramp,   XI.  615 
Side  gait,  Schiiller's,  IX.  456;  XIII,  796-7 
Sight,  p.  8;  I,  12 

Cortical  center  of,  p.  8;  XXI,  1307 

Loss  of,  VI,  358  to  64;  XIV,  808;  XXII, 
1331-S-6-7 

Perversion  of,  XIV.  808;  XXII,  1331-2-S- 
6-7 
Simple  delusional   insanity,   XVI,    1 1 13 

idiopathic    muscular    dystrophy,    X,  498; 
XIII,  787;  XVII,  1154 
Singer's  cramp,  XI,  615 
Singultus,  XII,  731 
Sinus  thrombosis,  II,  185;  XV,  966;  XVI,  1044 

Headache  in,  XV,  966 
Sixth    cranial    nerve    or    nucleus   (abducens), 

Symptoms  of  lesions  of,  XIV,  872 ;  XXII, 

1343 
Skill,  Loss  of:     See  apraxia 
Skin,  Diseases  causing  atrophy  of,  XVII,  II33 

eruptions  of,  XVII,   113S 

hypertrophy   of,   XVII,    1134 

trophic  lesions  of,  XVII,   1 124 

ulcerations  of,  XVII,   1136 

Glossy,  XVII,   1 160 
Skull  in  disease,  I,  22;  XVII,  1181:     See  also 

cranium 
Sleep,  I,  18 

Sleeping  sickness,  II,   142 ;   XVI,   105S 
Smell,  p.  8 

Cortical  center  of,  XIV,  810 

Loss  of,  VI,  356 

Perversion  of,  VI,  369,  390 

Tests  for,  I,  16 
Sneezing,  V,  313;  XII,  728 
Snow  blindness,  VI,  360;   XIV,  846 
Softening,  Cerebral,  X,  505-6;  XIV,  835-60-I ; 
XVI,  104.V65-6;   XVIII,   1207 

Brain  stem,  X,  534;  XII,  656 

Crus  cerebri,  X,  536-43 

Medulla,  X,  540-4;  XIII,  749 

Pons,  X,  538-43;   XIII,  749 

Spinal.  II,  189a;  X,  485-513-4-7-8-50; 
XIII.  793-8;  XIV,  827-30-1-8;  XV, 
080;  XVIII,  1211 


Somnambulistic  state.  III,  210;  XVI,  1061-72- 

3-5 
Somnolence,  II,  142;  III,  207;  XVL  1055 
Sopor,  III,  207 

Spasm,  I,  7;  XI,  570:     See  also  reflex  acts 
or  cramp,  p.  35 ;  IV,  242 
abdominal,  XII,  732 
asthmatic,  XI,  616-8;  XVII,  1194 
athetoid,  IV,  271 ;  XI,  574 
Auctioneer's,  XI,  615;  XII,  726 
Blepharospasm,     XI,     598,   616;    XII,   682, 

726 
Brachial,  XII,  733 
Choreic,  IV,  272;  XI,  573 
Clonic,  IV,  246 ;  XI,  571 
Cornet  player's,  XI,  615;  XII,  726 
Diaphragmatic,   XII,   731 
Facial,  XII,  726 
Glosso-pharyngeal,   XII,   727 
Habit.  IV,  274;  XI,  627 
Hypoglossal,    XII,    729 
Hysterical,  IV,  268;   XI,  586-618-20;  XII, 

637-732;  XVI,  1076 
Intercostal,  XII,  732 
Irregular,    IV,   247 
Jacksonian  epilepsy,  IX,  421  ;   XI,  587-8 

602-17;  XXI,  1304-5;  XXII,  131 1 
Jaw  muscles,   XII,  725 
Laryngismus  stridulus,   XI,  616;  XII,  728 
Local.  XI,  571-2;  XII,  637 
Lumbar,  XII,  733 
Mobile,  IV,  271 
Neck  muscles,  XII,  730 
Nictitans,   XII,  726 
Nutans,   XII,  679-90 
Occupation,   XI,   615 
Ocular  muscles,  XL  590;  XIV,  818-80-7 
Oesophageal,  XI,  616 
Phrenic,  XII,  73l 
Pianist's,  XI,  615 
Pneumogastric,   XII,  728 
Reflex.    IV,    268;    XI,    616-8;    XH,    637; 

XVII,   1154 
Salaam  cramp,  XII,  690 
Saltatory,  XI,  618 
Sciatic,  XII,  733 
Seamstress,  XI,  615 
Shoemaker's,  XI,  615 
Spinal  accessory,  XII,  731 
Telegrapher's,  XI,  615 
Tests  for.  I.  33 
Tic,   articulative,   XIII,   771 

convulsive,  IV,  267-70 ;  XI,  598  to  602- 
16;  XII,  726 

douloureux,    IV,    267;    XI,  599;  XII, 
726;   XV,  948 
Tonic,  IV,  245;  XL  572 
Torticollis,  XI.  618;  XH,  730 
Trigeminal,  XII,  725 
Typewriter's,   XI,  615 
Urethral,    XI,    616 


294 


INDEX 


Spasm.  Vesical,  XI,  6i6 

Whooping  cough,  XI,  6i6 
Writer's  cramp,  XI,  615 
Spasmus  glottidis,  XI,  616;  XII,  728 

mobilis,  IV,  271 :    See  athetosis 
nictitans,  XII,  679-90 
nutans,  XII,  679-cp 
Spastic  hemicrania,  XV,  930 

paralysis,  I,  33-9;  IV,  251;  X,  473 
paraplegia,  X,  525-47;  XIII,  800 
Special  senses,  Disturbances  of,  I,  I ;  XIV,  805 

syndromes  and  sypmtoms,   IX 
Speech,  p.  33 

Disorders  of,  11,  222  to  33;  XIII,  735 
Diseases  causing,  XIII,  735 
Tests  for  defects  in,  I,  8 
Sphygmomanometer,  I,  46 
Spina  bifida  and  occulta,  I,  23;  II,  loz;  X,  523 
Spinal  abscess,  II,  153-74-84 

Cerebro-spinal   fluid   in,   XIX,   1238 
accessory  paralysis,  XII,  705 

spasm,  XII,  730 
automatism   (Marie),   V,  327a 
caries,  II,  122 

column  in  disease.     See  vertebral 
cord,    endarteritis    and    thrombosis     and 
hemorrhage   of,    II,  147,  189a,  X, 
48s,  512-4-7-8-24-50;  XIII,  793-8; 
XIV,      827-30-1-8;       XV,      980; 
XVIII,  1211 
Localization   in:     See   localization 
Symptoms  of  lesions   of,   above  lum- 
bar enlargement,  X,  513-4-8-7-20- 
50;   XIII,   798;   XIV,  8301-1-8; 
XV,  980 
anterior     commissure,     XX,     1275 ; 
XXII,    1372 :  See    syringomy- 
elia 
horn,  XX,  1268;  XXII,  1324:  See 
poliomyelitis     and     progressive 
muscular   atrophy 
nerve  roots.  XX,  1279;  XXII,  1324: 

See  herpes  zoster. 

Burdach's    column    and    nucleus,  p. 

12;  XII,  654;  XIII,  786,  XX. 

1271 ;       XXII,        1322-60-3-4, 

1406 

Cauda    equina,    X,    487 ;    XII,    721 ; 

XV,  1007;  XXII,  1328 
cervical     enlargement,     X,     549    to 
52;    XIV,   838   to  40;  XXII, 
1330 

region,    X,    512    to  15;  XIV, 
830;   XXII,   1407 
conus  terminalis,  XIV,  833 
direct     cerebellar    tract,    XII,    647- 
53;  XX,  1272;  XXII,  1369-73, 
1406 
dorsal   region.   X,   516  to   19;   XIII, 

798;  XIV,  831;  XXII,  1404 
Goll's    column    and    nucleus,    p.   12 


Spinal,      lateral      column,     X,     525-47;     XII, 
653-60-95 ;        XIII,        800-1 ; 
XVIII,  1212;  XX,  1270-1-3-4; 
XXII,   1369-71-3-84-6-9,   1406 
lumbar     enlargement,     X,     484     to 
86;    XIII,    793;    XIV,   827-8; 
XVII,  1 149;  XX,  1329 
posterior     column,     X,     526;     XII, 
654-60;  XIII,  786;  XX,  1271- 
3;  XXII,  1360-3-4,  1406 
horn,   X,   1269;   XXII,   1322 
nerve     roots,     IV,     826;     XX, 
1278;    XXII,    1322 
postero-lateral     columns,     X,     526 ; 
XII.    660;     XIII,    799;    XX, 
1273;    XXII,    1406 
pyramidal    tract,    XX,    1270:        See 

also   lateral   column 
spino-thalamic      tract,     XX,      1274; 
See  also  lateral  column 
epilepsy.  I,  60-1  ;  IX,  433:  X,  509-20;  XIV, 

839  to  40 
ganglion,   lesion  of,   XX,   1277:     See    also 

herpes  zoster 
gumma,  XVIII,  1210 

hemiplegia,   IX.  432;   X,   509;   XIV,  844; 
XV,  982;  XX,  1276:  See  also  Brown- 
SequardTs    paralysis 
meninges.  Hemorrhage  in  the,  II,  147 
memingitis.   Acute  and   chronic,   XI,  605; 

XV,  974,   1005;   XVIII,   1213-4 
muscular    atrophy.    Peroneal    type    of,  X, 
496;   XII,  696 
Progressive,   X,   548 
Neuralgia.  XV,  971 ;  XVI,  1076 
or  neuritic  muscular  atrophy,  X,  496;  XII, 

696 
nuclei :     See  nuclei 
segment,   Lesions   of,   XIV,  826 

Localization  in:     See  localization 
syphilis,  XVIII,  1210-6 
tenderness,  IX,  425;  XVI,   1076 
tumor.    II.    152;    X,    486.    509-15-19-41-52; 
XIV,  828-39-40;   XIV,  975-82 
Spondylitis  deformans,    XV,  976 
Squint:     See  diplopia 
Stammering.  XII,  729;   XIII,  770 
Static  ataxia,   I,  42;   IV,  281;   IX,  438;  XII, 

642 
Status  epilepticus.  XVI,  1061 
Stellwag's   sign,    XVII,    1 192-3 
Sternutatio   spastica,   XII.   728 
Stereognosis,  Tests  for.  I,   n 
Stereotypy.  XVI,  1098,  iioi 
Stocking  form  of  anesthesia,  VI,  348;  IX,  415 
Stokes-Adams  disease,  XI,  582 ;  XVI,  1060 

phenomenon,  IX,  426 
Strabismus  convergens,  XIV,  872 
deorsum  vergens.  XIV,  874-7 
divergens.  XIV,  873 
sursum  vergens,  XIV,  875-6 


295 


INDEX 


Strumpel's  tibialis  phenomenon,   IX,  435 
Strychnine  poisoning,  V,  297;  VI,  366;  XI,  613 
Stupor,  III,  206;  XVI,  1097 
Stuttering,  XII,  729;  XIII,  771 
Subconsciousness,  p.  18 
Subcortical  lesions,  XXI,  1309 
Subscapular   paralysis,   XII,   711 
Suggestion.   Susceptibility  to,   in  hysteria,   IX, 

41s;  XVI,  1071-2-6 
Suicide  in  nervous  diseases,  I,  2 
Sulfonal  poisoning,  X,  482 
Sunstroke    or    heatstroke,  XI,  589;   XV,  968; 
XVI,  1070 
Convulsion  in,  XI.  589 
Headache  in,  XV,  968 
Superficial  reflex  acts,  I,  57 ;  V,  297 
Superior   laryngeal   paralysis,    XIII,   757 
oblique  muscle.   Paralysis  of,  XIV,  876 
rectus  muscle,   Paralysis  of,  XIV,  874 
Supinator  longus.  Paralysis  of,  XII,  716 
Supra-orbital  neuralgia  or  neuritis,  XV,  944*53 

-scapular   paralysis,    XII,    708 
Surface  thermometers,  I,  78 
Sweating,  Excessive,  XVII.  1203 
Sydenham's  chorea.  II,  113,  126;  XI,  622-3 
Symmetrical  gangrene.  XV,  ion;  XVII,  1195 
Sympathetic    ganglionic    system.    Irritation    of 
the,  XVII,   1143-92 
Diseases  of  the,   XVII,    1 122-9-30 
Paralysis  of  the,  XVII,  1142-91 
Symptom    complexes    and    special  syndromes, 

IX 
Symptomatic  neuralgia,  XV,  937-53 
epilepsy,  XI,  576  to  596 
mania.  XVI,   11 14 
melancholia,   XVI,    11 15 
Syncope,   Coma   from,   XVI,   1059 

Local,   XVII,    1105:     See   also  Raynaud's 
disease 
Syndromes  and  special  symptoms,  IX 
Synergy,  I,  42;  IV.  jS:-2 
Synkinesiae,  X,  47,; 

Syphilis,  I,  2:     See  al«'.  cerebro-spinal  syphilis 
Argyll-Robertson  phenomenon  in,  V,  332; 

IX,   437;    XIV,   Sgt 
Cerebro-Spinal,    II,    108,    175    to  79,  180; 
XVIII,  1214;  XIX,  1232 
fluid     in,     VIII,    409-12-3-4;    XVIII, 

1205;   XIX,    12,30-1-2 
Optic  neuritis  in,  XIV,  903 
Vertigo  in,  XV,   1025-33 
Endarteritis   and    thrombosis    in,    II,    175 ; 

XVIII,   1207-11 
Lateral  sclerosis  in,  X,  525;  XVIII,  1212 
Syphilitic    Meningitis.    IT.    176;    XV,    952-81; 
XVIII.    i2o8-f)-T.vr4 
Cerebral  of  base,  XVIII,  1209 

of    convexity,    XVIII,    1208 
Cerebro-spinal,   XVIII,    1214 
Spinal.  XVIII,   1213 


Sj-philitic,     nervous     diseases,     II,     94,     108; 
XVIII,   1205 
neuralgia,  XV,  952 

neuritis,  II,  177;  XV,  952;  XVIII,  1215 
Syphilophobia,  III,  235;   XVI,   1074-S 
Syringomyelia,  X,   553;   XII,  693;   XIII,  802; 
XIV,    840-2;    XV,  1009;  XVII,  1151- 
70-87;    XXII,    1370-2 

Tabes   dorsalis,  II,   134-79;     VIII,    409-12-13; 

IX,  423;  xn,  661;  XIII,  759-85;  XIV, 

829-71- a5,  912;  XV,  979-88,  1004;  XVIII, 
1217;  XIX,  1231 

Argyll-Robertson  phenomenon  in,  V,  332; 
IX,  437;  XIV,  891 

Arthropathy  in,  XVII,  1186 

Cerebro-spinal   fluid   in,   VIII,   409  to   14; 
XVIII,  1217;  XIX,  1231 

Crises  in,  IX,  423;  XV,  988;  XVI,  1062a 

Cuirass  in,  VI,  348;  XIV,  829 

Optic  atrophy  in,  XIV,  912 

Perforating  ulcer  in,  XVII,   II72 

Vertigo  in,  XV,   1015 

vision,  Limitation  of  field  of,  in,  XIV,  871 
Tachycardia,  XII,  704;  XVII,   1193 
Taches  Cerebrales,  V,  327 ;  XI,  590 
Tactile  saisations,  p.  6 

Tests  for,  I,  48 
Talalgia,  XV,   1002 
Tapir  mouth,  X,  497 
Taste,  I,  17 ;  VI,  357-70-91 ;  XIV,  810 

Cortical  center  for,  XIV,  810 

Diseases  causing  disorder  of,  XIV,  810 

Tests  for,  I,  17 
Tecto-spinal  tract.  The.  p.  9 
Telegrapher's   cramp.    XI.    615 
Temperature   sense,   p.   6 

Exaggeration   of,   VI,   368 

Loss  of,  VI,  350 

Tests  for,  I,  55 
Temporal  convolution,  Lesions  of  the  superior, 
XIV.  g25;  XXI,  1306;  XXII,  1382 

Lesions  of.  causing  deafness,   XIV,   1306 ; 

Localization  in  :     See  localization 

Sensoiy   aphasia   in.    XXII,    1358-82 
Tendon   reflex  acts,  V,  299 

exaggerated,    Diseases    causing,    X,    473; 
XIV,  8ii 

diminished,   X,  472;   XIV,   811 

Tests  for,  I,  60-6 
Tenesmus,  XI,  616 
Terminal  dementia,   XVI,   1105 
Tetanus,  II,  172;  XI,  603 

neonatorum,  XI,  603 
Tetany,  U,  121 ;  XI,  612 
Tetartanopia,  VI,  363;     XIV,     856-7;     XXI, 

1.307;  XXII,  1356 
Thalamo  spinal  tract.  The,  p.  9 
Thermalgia,  XV,  1003a 
Thermic  anesthesia,  VI,  350;   XIV,  81 1-2 

hyperalgesia,  VI,  368 


296 


INDEX 


Thermic,  hyperesthesia,  VI,  368 

hypesthesia,   VI,   350 
Thermometry  in  examination  of  nervous  dis- 
eases. I,  78 
Third    cranial    nerve    nucleus,    Symptoms  of 
lesions    of,    XXII,    1339-42:  See   also 
localization 
Thomsen's  disease,  II,  ic6;  IV,  265;  XI,  611 

Muscular  hypertrophy  in,  XVII,  1157 
Thoracic   paralysis,    XII,    709-10 
Thought,  p.  24 

Thrombosis,  Cerebral,  X,  506;  XIV,  835-60-1; 
XVI,  1066;  XVIII,  1207 
Posterior  inferior  cerebellar  artery,  XXI, 

I2gi 
Sinus,  II,  185;  XV,  966;  XVI,  1044 
Spinal,  XVIII,  121 1 
Thymus  gland.  Lesion  of,  IV,  253;  X,  554 
Thyroid  gland,  Lesion  of,  I,  20;  II,  132;  IV, 

253:  Xn,  672;  XVn,  1 193 
Thyreo-ary-epiglottis  paralysis,  XII,  757-60-2 
Tibialis   paralysis,    XII,   720 
Tic,  articulative,  XIII,  771 

convulsive,    IV,    267-70;    XI,    598    to  602, 

616;  XII,  726 
douloureux,   IV,  267;   XI,  599;   XII,  726; 
XV,   94S 
Tingling,  VI,  375 
Tinnitus  aurium,  I,  15;  VI,  388 
Tobacco  vertigo,  XV,   1031 
Toes,  Clubbed  fingers  and,  XVI,  1184 
Tongue,  Paralysis  of,  XII,  706 

Spasm  of  muscles  of,  XII,  729 
Tonic  spasm,  IV,  245 

Diseases   causing,   XI,   572 
Tonicity,  Muscular,  I,  40;  IV,  240;  X,  472-3 
Tonometer,  I,  46 

Tooth-Charcot-Marie   type   of   muscular   atro- 
phy, X,  496;  XII,  696 
Topoanesthesia,   VI,   376 
Torticollis,  XI,  598,  618;  XII,  730 
Toxic  coma,   XVI,   1069 
convulsion,  XI,  595-6 
headache,  XV,  965 
insanity,    XVI,    mo 
nervous   diseases,   II,  92 
tremor,  XII,  673 
vertigo,   XV,   1030 
Trance.  XVI,  1071 
Transcortical  aphasia,  XIII,  778 
Transference  of  hysterical  anesthesia,  IX,  415; 

XIV,  837;  XVI,  1076 
Transmission,  nervous,  p.  6 
Transverse  myelitis,  XV,  980 :  See  myelitis 
Traumatic  nervous  diseases,  I,  i ;  II,  91,  136-46 
hysteria,   XVI,   1077 

neuroses,    II,    157;    XII,    674;  XV,  1034; 
XVI,  1077 

vertigo  from,   XV,   1034 
tetanus,  XI,  603 


Tremor,    p.    37;    II,    163;  IV,  250;  XII,  639; 
XXI,  1292-4 

Alcoholic,  XII,  673 

Asthenic,  XII.  671 

Diseases  causing,  XII,  639 

Essential,  XH,  681 

Hysterical,  XII,  674 

Intention,  IV,  291 ;  XII,  645 
Diseases  causing,  XII,  645 

Mercurial,  II,  160;  XII,  673 

Neurasthenic,    XII,    671-4 

Nicotine,   XII,  673 

Opium,  XII,  673 

Passive,  IV,  290;   XII,  646-61 
Diseases  causing,  XII,  646-61 

Senile,   XII,   678 

Tests   for,   I,  32 

Toxic,  XII,  673 
Trident  shaped   hand,   XVII,   1177 
Trigeminal    or    trifacial    neuralgia  or  neuritis, 
XV,  943  to  48 

paralysis,  XII,  702 

spasm  or  cramp,  XII,  725 
Trional   poisoning,   X,  482 
Trismus,   IV,  265;   XII,  725 
Trochlearis  paralysis.  XII,  701 
Trophic  influences,  p.  38 

lesions,   Diseases  causing,  XVII,   1121-8 
Tests  for.  I,  41 
Trophedema,  XVII,   1202 
Trousseau's  sign,  IX,  440;  XI,  612 
Trypanosomiasis,   II,   142;   XVI,   I055 
Tuberculosis  in  nervous  diseases,  I,  2 
Tuberculous    meningitis,    II,    119-23-92;     XI, 
593;   XIX,   1228-9 

Cerebro-spinal  fluid  in,  XIX,  1228-9 
Tumor,  II,  152-91 

of  brain  stem,  X,  53S-7-9-4I-2;  XII,  656; 

XIII,  749 
Cerebellar,  XIV,  909 

Cerebral,   II,    125-52-91;   X,  507-35-7-9-4I ; 

XI.  578-87;  XIV,  836-52-9-62-4-5,  908; 

XV,  061 :  XVI,  1033-50 
Cerebro-spinal   fluid   in,  VIII,  405-12-3; 

XIX,   1237 
Coma  in,  XVI,  105c 
Headache  from,  XVI,  1050 
Perversion  of  vision   in,  XIV,  852-9-62- 

4-5 
Vertigo  in,  XV,  1033 
Spinal  cord,  II,  152-91;  X,  486,  509-15-19; 

XIV,  828-3Q-40-2 :  XV,  975-82,  1006 
of   cervical   enlargement,   X,   552;   XIV, 

839 
region  of  spinal  cord,  X,  509-15-19 

dorsal  region,  X,  519 

lumbar    enlargement,    X,    486;    XIV, 

828;   XXII,   1329 

cms  cerebri,  X,  537;  XII,  656 

medulla  oblongata  X,  541 1  XII,  656 

optic  chiasm,  XIV,  864-5 


297 


INDEX 


Typewriter's  cramp,  XI,  615 

Typhus    fever,    Cerebro-spinal    fluid  in,  XIX, 

1236 

Ulcer,   Perforating,   XVII,    1172 

Ulcerations,      Diseases      causing      cutaneous, 

XVII,   1136 
Ulnar  paralysis,  XII,  715 
Umbilical  reflex,  V,  309 

Tests  for,  I,  57 
Unconsciousness,  I.  3 ;   III.  201 
Understanding,  I,  6;  III,  202 
Unequal  pupils,  V,  341  ;   XIV,  820 
Unverricht's  family  myoclonus  epilepticus,  XI, 

601 
Upper  motor  neurons,  p.  9;  IX,  461 

sensory  neurons,  IX,  463 
Uremia,  II,   193 

Cerebro-spinal    fluid   in,    XIX,    1243 
Uremic  amaurosis,  XIV,  853 

coma.   I,   193;   XVI,   1068 

convulsion,   IX.  576-81 

headache,  XV,  957 
Urethral  crises,  IX,  423 
Urethral   spasmodic  stricture,  XI,  618 
Urophobia,  III,  235;   XVI,   1074-5 
Urticaria,    XVII,    1167 

Angio-neurotic.    XVII,    1201 

scripta,  XVII,   1167,   1201 
Uvular  reflex,  V.  315 

Tests  for,  I,  58 

Vagus  paralysis,  XII,  704;   XIII,  763 

spasm,  XII,  728 
Valleix,    Points   of.    XV,   937-43-9-77-90-5-7 
Vascular   disorders.    Diseases   causing,    XVII, 

1144-S 
Vaso-niotor       disorders,       Diseases      causing 
XVII,   1 130 
reflex  acts,  V,  301-27 
Tests  for,   I,  59 
Venery  in  nervous  diseases,  I,  2 
Vertebral  column  in  disease,  I,  23 
Vertex  headache,  XV,  953 
Vertige  paralysant,   XV,   1032 
Vertigo,  I,  I :  VI,  392 ;  XV,  932 
Alcoholic,  XV,  103 r 
Apoplectic,  XV,  1027 
Atheromatous,   XV,    1025 
Aural,  XII,  649-85;  XIV,  918;  XV,  1019 
in  brain  stem  lesions,  XV,  1017 
Cardi.ic,   XV,    1024 
in  cerebellar  disease,   XV,   1016 
cerebral  anemia,  XV,  1021-3-4-5 
congestion,  XV,  1026 
tumor,  XV,  1033 
CoflFec.  XV,   103 r 

in  digestive  disturbances,  XV,  1023 
Diseases  causing,  XV,  932 
Drug,  XV,  1031 


Vertigo,  Epileptic,  XV,  1028 

Exhciustion,  XV,   1022 

in   fourth   ventricle  lesions,   XV,   1018 

Gerlicr's  disease,  XV,  1032 

Hysterical,   XV,   1034 

Labyrinthine,  XII,  649-85;  XIV,  918;  XV, 
1019 

Laryngeal,  IX,  423;  XVI,  106a 

Meniere's,    XII.    649-85;    XIV,  918;    XV, 
1019 

in  meningitis,  XV.   1033 

Migrainous,    XV,    1029 

Morphine,  XV,   1031 

Neurasthenic,    XV,    1034 

Nicotine,  XV,  1031 

Ocular,   Xn,  648;   XV,   1020 

Paral>sing,  XV,  1032 

Quinine,   XV,    1031 

Tabetic,  XV,  1015 

Tobacco,   XV,    1031 

Toxic,  XV,   1030 

in  traumatic  neuroses,  XV,   1034 
tumor,  XV,  1033 
sclerosis    (disseminated),   XV,    1015 

Syphilitic,    XV,    1025-33 

with  ataxia,  XII,  648-9;   XV,   1015-20 
Vesical  crises,  IX,  423 

reflex,  V,  324 

spasm,  XI,  616 
Vestibulo-spinal   tract,   The,  p.    9 
Vibration  sense.  Loss  of,  VI,  353 

Tests  for,  I,  56 
Violinist's  cramp,   XI,  615 
Visceral   crises,   IX,  423 

Vision,  Diseases  causing  disturbances  of,  XIV, 
808;   XXII,   1331 

Double,  XIV,  818:  See  also  diplopia 

Green,   XIV,  847 

Limitation  of  field  of,  IX,  415;  XIV,  817- 
68  to  71 ;  XVI,  1076 

Localization    of    lesions    causing    disturb- 
ances of.  XXII.  1331 

Loss  of.  XIV,  852a  to  55;  XXII,  1334 

Perversion  of,  XIV,  816 

Red,  XIV,  846 

Tests  for,  I.   12-3-4,  29 

Yellow,   XIV,  945 
Visual  aphasia,  III,  224;  XIII,  776 

axis,  displacement  of,  I,  29;  XIV,  818 
Vitiligo,  XVII,  1 162 
Vocal  cords.  Paralysis  of,  XIII,  757-9 
Voltoni's   disease,   XV,   1019 
Voluntary  motion,  p.    14,  31 

Disorders  of,  IV,  240;  X,  XI;  XII;  XIII 
Vulvo-vaginal  crises,  IX,  423 

Walk,  Inability  to,  in  disease,  I,  21 ;  XIII 
Wasserniann    reaction,    VIII,    413 ;   XII,  66r ; 

XIII,   78s;   XIV,  829,  871,  912;   XV, 

9791,   XIX,   1232 


298 


INDEX 


Weakened  mentality,  Diseases  causing,  XVI 
Weakness,  XIII,  792 

Tremor  from,  XII,  671 
Weber's  law,  p.  16 

syndrome,  IX,  440;  XXI,  1293 

Tests,  I,   IS 
Werding-Hoflfman    type    of    poliomyelitis,     X, 

548a 
Wernicke's    polioencephalitis    superior  hemor- 
rhagica acuta,  X,  543;  XVI,   1048 

predilection  muscles,  IV,  254;  X,  504 

scheme   of  aphasia,   XIII,   739 
Westphal-Edinger's  nucleus,  V,  329 

pupillary  reflex,  V,  337 

pseudo-sclerosis,    XII,   667 
Whooping  cough,  XI,  616 
Will,  p.io 

Free,  p.  10 

power,  p.  10 
Word    blindness,    III,  229;    XIII,    777;  XXI, 
1307;  XXII,  1381 


deafness.    III,   223-33;    XIII,   775;    XXII, 
1306;  XXII,  1382 
Worry,  I,  I 

Wounds  as  etiological  factors,  II,  146 
Wrist-drop,  X,  494;  XI,  584;  XII,  716;  XIII, 
790;  XVI,  1053 
reflex,  V,  322 
Tests  for,  I,  64 
Writer's  cramp,  XI,  615 

Writing,    Diseases   causing   disorders  of.  III, 
227-8;  XIII,  735-79-80;  XXII,  1401 
Tests  for  defects  in,  I,  10 
Wry  neck,  XII,  730 

Xanthopsia,   XIV,  845 

1 
Yawning,  XII,  731 
Yellow  vision,  XIV,  845 

Zone  of  language,  p.  35 


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